Biochemistry and Biophysics Reports

Cancer is a complex disease characterized by genetic and molecular diversity, often involving dysregulation of critical cellular pathways. Recent advances in pan-cancer research have highlighted the importance of shared oncogenic mechanisms across different cancer types, providing new avenues for therapeutic exploration. Protein kinases, particularly those involved in phagocytosis, play pivotal roles in cellular homeostasis and immune response. This study systematically examines the genetic alterations and expression profiles of protein kinases associated with phagocytosis across various cancer types, using data from The Cancer Genome Atlas (TCGA) and other publicly available resources. We analyzed single nucleotide variations (SNVs), copy number variations (CNVs), methylation patterns, and mRNA expression to identify recurring alterations and their associations with survival outcomes. Our findings reveal that MET and MERTK are the most frequently mutated genes, with missense mutations dominating across cancers. CNV analysis shows significant correlations with survival in cancers like UCEC, KIRP, and KIRC, while methylation analysis indicates cancer-specific regulatory patterns affecting gene expression. Differential expression analysis highlights distinct cancer-type-specific expression profiles, with genes like MET and BTK displaying significant variation. Crosstalk pathway analysis further reveals the involvement of these kinases in key cancer-related pathways, such as epithelial-mesenchymal transition (EMT) and apoptosis. Drug sensitivity analysis identifies potential therapeutic targets, with gene expression correlating significantly with cancer cell line responsiveness to specific compounds. These findings underscore the importance of the phagocytotic kinome in cancer biology and suggest potential therapeutic strategies targeting protein kinases to enhance immune response and improve treatment outcomes.

BackgroundPancreatic cancer is a deadly cancer around the world. To reduce side effects and enhance treatment efficacy, study on combination therapy for pancreatic cancer has gained much attention in recent years. MethodsIn this paper, we propose a novel triple treatment combining propolis and two physical stimuli-thermal cycling-hyperthermia (TC-HT) and low-intensity ultrasound (US) on a human pancreatic cancer cell line PANC-1. MTT assay was used to determine the viability of PANC-1 cells. Flow cytometry was used to detect apoptosis, mitochondrial membrane potential (MMP) loss, and intracellular reactive oxygen species (ROS) levels. Western blot analysis was further performed to measure protein expression and phosphorylation. ResultsThe experiments found that, after the triple treatment, the cell viability of the PANC-1 cells decreased to a level 80% less than the control, without affecting the normal pancreatic cells. Another result was excessive accumulation of ROS after the triple treatment, leading to the amplification of apoptotic pathway through the mitogen-activated protein kinase (MAPK) family and mitochondrial dysfunction. Moreover, the combination of TC-HT and US also promotes the anticancer effect of the heat-sensitive chemotherapy drug cisplatin on PANC-1 cells. ConclusionThis study, to the best of our knowledge, is the first attempt to combine TC-HT, US and a nature compound in cancer treatment. We demonstrate that physical stimuli could augment the therapeutical effect of anticancer agents. It is expected that optimized parameters for different agents and different types of cancer will expand the methodology on oncological therapy in a safe manner.

Chromatin is a highly dynamic entity of the eukaryotic cell nucleus. New evidence is emerging in support of the notion that chromatin can locally and globally rearrange itself to adapt with the cellular microenvironmental changes. Such changes include oxidative stress such as supraphysiological oxygen level, found in hyperoxia. Although it is known that hyperoxia can result in DNA damage and alterations in cell function, it is not well understood how the chromatin architecture changes under such a condition and what the functional significance of such change entails. In this work we developed an imaging-based technique to visualize and characterize nanoscale chromatin remodeling under hyperoxia, created via hydrogen peroxide treatment. We found high spatiotemporal variability of remodeling in different chromatin domains such as the euchromatin, heterochromatin and interchromatin. Chromatin remodeling was hindered by the GSK126 mediated inhibition of methyltransferase EZH2, which regulates the chromatin compaction. Epigenetic modifications and DNA damage under hyperoxia was investigated, which was found affected by the pretreatment of GSK126. The developed techniques and findings inform us with new mechanistic insights of chromatin remodeling which might lead to new intervention strategies to target genotoxic hyper-oxidative stress, which is common in degenerative diseases and aging, and for cell therapy in regenerative medicine.

The interdependence of sleep and overall well-being is profound. Sleep has the capacity to regulate hematopoiesis, thereby sustaining our physiological equilibrium. Nevertheless, our understanding regarding the potential reversibility of this regulatory process remains limited. In this study, we present evidence suggesting that exposure to middle-infrared radiation (MIR) within the 5-7 mm wavelength range can elicit non-thermal biological effects within the human body. These effects are characterized by an augmentation in blood circulation, mediated through modifications in red blood cell properties. Furthermore, MIR exposure is accompanied by a reduction in homocysteine levels and suppressor T-cell populations. Importantly, daytime modulation of MIR has been shown to significantly facilitate the amelioration of insomnia symptoms during nighttime, primarily through its impact on the architecture of deep sleep. Conclusively, our investigation reveals a robust association between cardiometabolic function and human sleep, with MIR presenting a promising avenue for enhancing sleep quality by regulating both the circulatory system and the immune system. These findings pave the way for the development of therapeutic strategies aimed at mitigating prevalent sleep-related disorders by disentangling the intricate links between sleep and cardiometabolic function.

Radiosensitivity, the susceptibility of cells to ionizing radiation, plays a critical role in understanding the effects of radiation therapy and exposure on tissue health and regeneration. Identifying characteristics that predict how a patient may respond to radiotherapy enables clinicians to maximize the therapeutic window. Limited clinical data suggested a difference in male and female radiotherapy outcomes. Radiotherapy for gastrointestinal malignancy is still a challenge due to intestinal sensitivity to radiation toxicity. In this manuscript, we demonstrated sex-specific differences in intestinal epithelial radiosensitivity. In mice models of abdominal irradiation, we observed a significant increase in oxidative stress and injury in males compared to females. Lgr5+ve intestinal stem cells from male mice showed higher sensitivity to radiation-induced toxicity. However, sex-specific differences in intestinal radiosensitivity are not dependent on sex hormones as we demonstrated similar sex-specific radiosensitivity differences in pediatric mice. In an ex-vivo study, we found that human patient-derived intestinal organoids (PID) derived from males showed higher sensitivity to irradiation compared to females as evidenced by loss of budding crypt, organoid size, and membrane integrity. Transcriptomic analysis of human Lgr5+ intestinal stem cells suggested radiation induced upregulation of mitochondrial oxidative metabolism in males compared to females possible mechanism for radiosensitivity differences.

Withdrawal statementThe authors have withdrawn this manuscript because the operation process of animal tumors does not comply with relevant ethical requirements. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author.

Tumor Treating Fields (TTFields) are low-intensity, intermediate-frequency alternating electric fields that exert antimitotic effects on cancer cells. This study evaluated the in vitro efficacy of TTFields on biliary tract cancer (BTC) cell lines HCCC-9810 and RBE, investigating their sensitivity to TTFields across varying frequencies and electric field intensities. The results demonstrated that a frequency of 150 kHz induced the most pronounced cytotoxic effects, significantly impairing clonogenicity and migratory capacity while inducing abnormal mitotic processes. Furthermore, TTFields treatment triggered a marked upregulation of immunogenic cell death (ICD) biomarkers, including enhanced surface exposure of calreticulin (CRT) and increased extracellular release of high mobility group box 1 (HMGB1) and ATP. These findings indicate that TTFields represent a promising therapeutic approach for BTC, not only by suppressing tumor proliferation but also by enhancing ICD.

BackgroundRadiation-induced cardiac injury results in complex clinical presentations, unique management issues, and increased morbidity and mortality. But the underlying mechanism of radiation-induced cardiac injury is still unclear. The aim of this study is to explain the compositional alterations of innate and adaptive cells after thoracic irradiation and the relationship of macrophage with other adaptive cells. MethodsC57BL/6 mice were anesthetized and performed with 20Gy single dose cardiac irradiation. We carried out mice echocardiography to examine cardiac function. Masson and immunohistochemical staining were adopted to analyze cardiac fibrosis. Blood and cardiac tissue were collected 7 days, 4 weeks and 8 weeks after irradiation and sham-irradiated mice were set as a control group. Part of blood and tissue samples were analyzed with mass cytometry. We also used remaining blood samples to measure pro-fibrotic cytokines. ResultsWe observed reduced cardiac diastolic function and pathologically confirmed cardiac fibrosis after thoracic irradiation. Through mass cytometry, we identified that the proportion of neutrophils, macrophages and monocytes elevated. The ratio of T and B cells decreased after irradiation in the blood samples. For tissue samples, the proportion of macrophages, monocytes and neutrophils increased, endothelial cells reduced, but T and B cells also increased. The level of TGF-{beta}, TNF-, IL-6 climbed considerably, all of them are closely associated with the evolution of macrophage function during recovering phase of cardiac injury. In the correlation plot, we also discovered that CD4+T and CD8+T cells were strongly positively correlated with macrophages. ConclusionWe illustrated the immunological response after radiation-induced cardiac fibrosis, and macrophage may play a crucial role during the process. The results might have therapeutic potential for targeting macrophages in order to reduce radiation-induced cardiac fibrosis.

BackgroundLocalized and total body irradiation are used to treat certain cancers and also used prior to transplantation of stem cells or organs. However, the use of radiation also induces collateral damage to the cells of healthy tissue. Although the acute damage of radiation to oocytes is well known, the long-term effects induced by radiation to stromal cells and their relationship with age are still unclear. MethodsA total of 206 two-month-old female mice were whole-body exposed to gamma rays at doses of 0, 0.5, 1, 2, or 4 Gy, respectively. The mice were sacrificed at 3.5, 9, 12, or 18 months of age and pathological changes including cysts and tumors were assessed in the ovary and other organs. ResultsThe overall incidence of visible pathological changes of mice receiving irradiation was 33.7% in the ovary, but much lower in the liver, spleen, lung, thymus, and skin. Among these, the ovarian cyst formation rate was 24.7%, and tumor lesions were 10.2%, respectively, compared to 5% cyst formation and no tumor lesions among control, unirradiated mice. Statistical analysis showed that cyst formation was age, but not dose-dependent, whereas the formation of tumor lesions was dependent on both age and radiation dose. Pathology analysis indicated that most ovarian cysts originated from follicles and both tumor lesions analyzed originated from granulosa cells. ConclusionOvaries are highly susceptible to the effects of radiation. Long-term damage is increased after total body irradiation in mice, manifested by higher incidences of cyst formation and tumor lesions. The ovarian stromal-derived granulosa cells might play an essential role in these changes.

Granulosa cells (GCs), as the largest somatic cell group in follicles, provide nutrients and microenvironment for oocyte growth and maturation. GC proliferation and apoptosis are influenced by several genes, with the Kruppel Like Factor 12 (KLF12) gene contributing to the modulation of several cellular activities. Nevertheless, the precise modulatory function of this gene within the context of ovarian GCs remains unelucidated. We cloned the KLF12 gene of New Zealand female rabbits, and evaluated its expression and localization in the ovaries of female rabbits of different ages by quantitative real-time PCR (qRT-PCR) and fluorescence in situ hybridization (FISH). In order to determine the role of KLF12 in ovarian GCs, we used qRT-PCR, WB, CCK-8 and Annexin V-FITC/PI to detect the effect of KLF12 on GCs proliferation and apoptosis. The coding sequence of KLF12 gene of New Zealand female rabbit was predicted and cloned for the first time in this study. The coding region was 1209 bp, encoding 402 amino acids. KLF12 overexpression has a negative effect on the proliferation and cell cycle progression of rabbit GCs. KLF12 knockdown partially rescues GCs proliferation, accelerates GCs cycle progression, and promotes Estradiol (E2) and Progesterone (P) secretion. In addition, KLF12 was also proved to be a key regulator of PI3K/Akt signaling pathway in GCs. In conclusion, the study provides evidence that KLF12 plays a pivotal role in the maturation and proliferation of ovarian GCs in female rabbits. This work establishes a conceptual foundation for investigating deeper into the possible regulatory mechanisms underlying follicular development and growth. Author summaryGCs are essential for oocyte growth, not only providing necessary nutritional support for oocyte growth and maturation, but also constructing a key microenvironment. In this study, the biological function of KLF12 gene was systematically elucidated in rabbit for the first time. It was found that KLF12 inhibited follicular development by negatively regulating GCs proliferation and cell cycle. Combined with its effect on E2 and P secretion, the important regulatory role of KLF12 in follicular maturation and hormone balance was revealed. These innovative findings not only deepen the understanding of the regulatory network of ovarian development, but also provide a new theoretical basis for the basic research of reproductive biology. More importantly, it provides a potential molecular target for the development of new technologies to improve the reproductive efficiency of livestock. It also provides a valuable reference model for the study of the mechanism of human reproductive dysfunction related diseases.

1.IntroductionWorldwide, cancer is a significant public health problem. Curcumin exhibits anti-inflammatory, antiproliferative, and anticancer properties when used in medicine. Investigated study for Curcumins chemopreventive mechanism against human malignancies, this research examined the cellular and molecular alterations generated by curcumin modified compound in breast cancer (MCF-7) cell lines. Oncogenic EGFR and VEGFR2 mutations lead to the formation, invasion, and maintenance of malignant phenotypes in humans, including breast cancer. Studied prognostic markers such as C-myc and Ki67 in breast cancer, and the apoptotic gene as Caspase-3 have been done. Aim of the workThe purpose of this study is to determine the therapeutic efficacy of curcumin nanoparticles and nanocapsules in breast cancer cell lines (MCF7). Materials and methodsWe used real-time PCR to assess the expression of the C-myc, Ki67, EGFR, VEGFR2, and Caspase-3 genes in MCF7 cells treated with Curcumin nanoparticles and nanocapsules. ResultsCurcumin nanoparticles and nanocapsules boosted apoptotic cell populations considerably regardless of the nanotechnology used. Additionally, the mRNA expression analysis results indicated that the mechanism activated by curcumin nanocapsules involved the upregulation of the oncogenes EGFR and VEGFR2. In comparison to curcumin nanoparticles, curcumin nanocapsules significantly reduced the expression of Ki67 and c-myc mRNAs in breast cancer cells. The mRNA expression study revealed that curcumin nanocapsules produce an increase in the apoptotic Caspase-3 gene production compared to cells treated with curcumin nanoparticles. ConclusionThis work demonstrates that curcumin nanoparticles created using a novel mechanical process can be employed successfully as an anticancer agent. These findings add to our understanding of the molecular mechanisms behind curcumin nanocapsules anticancer activity in breast cancer.

BackgroundGene expression profiling in radiation-exposed blood is a valuable tool for biodosimetry and clinical research. Evaluating the bloods transcriptomic radiation response provides insight into absorbed dose, hematotoxicities, and immune reactions. However, detailed analysis using long-read RNA sequencing is currently limited in its diffusion, despite the potential additional insights that could be extracted, including novel isoform discovery and on-the-field gene expression studies, owing to its portability. ResultsIn this study, we utilized Oxford Nanopore Technologies long-read RNA sequencing on human whole-blood samples from three healthy donors 6 hours after exposure to 4 Gy of X-rays. Compared to sham-irradiated (0 Gy) blood, gene-level differential expression analysis identified 117 upregulated and 66 downregulated genes, including canonical DNA damage repair and inflammatory responses. At the transcript level, 102 transcripts were significantly upregulated, and 17 were downregulated, revealing isoform-specific regulation that was not captured at the gene level. Notably, IL32, which showed no significant change at the gene level, exhibited strong upregulation of two transcript isoforms, while WDR74, ITM2B, AK2, and RPS19 displayed changes in transcript usage following irradiation. Leveraging the power of long-read RNA sequencing, we further identified 26 novel transcript isoforms, expanding the catalog of radiation-responsive transcripts. ConclusionsThis is the first comprehensive study of long-read RNA-seq for transcriptomic profiling of human whole blood following ionizing radiation. These findings highlight the ability of long-read RNA sequencing to provide a more detailed view of radiation-induced transcriptomic alterations, underscoring its potential for biodosimetry and clinical applications.

Breast cancer is the first cause of cancer death in women all over the world. And the morbidity of breast cancer has been increasing in recent years. Nowadays, the treatment of breast cancer is still a problem. Radiotherapy resistance is one of the important factors leading to poor prognosis of clinical treatment. Curcumin, a plant polyphenol from Curcuma longa, has antitumor activity and inhibition of tumor recurrence and metastasis. However, the influence of curcumin on radiosensitivity of breast carcinoma xenografts, the synergistic effect and possible mechanism of curcumin and Glucose-Gold nanoparticles (Glu-GNPs) in nude mice in vivo need to be further explored. The model of transplanted tumor in nude mice was established and sensitized by intravenous injection of curcumin and Glu-GNPs. The results showed that curcumin can significantly inhibit the growth of tumor, and has no obvious effect on the body weight of nude mice, and Curcumin, Glu-GNPs and X-ray irradiation treatment alone or in combination could reduce the expression of VEGF and HSP90 mRNA and protein compared with model group in tumor tissue. The inhibition of irradiation resistance may be related to inhibiting the synthesis of VEGF and HSP90. This study suggested that curcumin and Glu-GNPs have the radiosensitization effect in vivo, which provides an experimental basis for the clinical development of green radiosensitizers.View Full Text

We propose a technique of controlled manipulation with mammalian intracellular bodies by means of optical trapping in order to reveal viscoelastic properties of cell interior. Near infrared laser in the spectral range of tissue transparency was applied to study dynamics of the nucleolus-chromatin complex inside the thermodynamically non-equilibrium system of a mouse oocyte. A nucleolus of germinal vesicle (GV) oocyte as spherical probe was displaced from the equilibrium and its relaxation dynamics was observed. We developed software for subdiffraction tracking of a nucleolus position with lateral resolution up to 3 nm and applied it for different GV-oocyte chromatin configurations. We showed differences in viscoelastic properties within nucleoplasm of NSN-oocytes, visualized by Hoechst 33342 staining. Also, we demonstrate that in germ cells basic biophysical properties of nucleoplasm can be obtained by using optical trapping without disruption and modification of cellular interior.

Ultrahigh dose rate radiotherapy (FLASH-RT) is under intensive investigation for its biological benefits. The mechanisms underlying its ability to spare normal tissues while suppress tumor growth still remain controversial. Here we reveal that compared to the low dose rate electron irradiation (0.36 Gy/s), FLASH electron irradiation at 61 or 610 Gy/s enhances the cytochrome c leakage from mitochondria in human breast cells MCF-10A, which elicits substantial caspase activation, suppresses both the cytosolic mitochondrial DNA (mtDNA) accumulation and IFN-{beta} secretion. Besides, the deletion of mtDNA severely decreases the radiation-induced cGAS-STING activation. Conversely, the cytochrome c leakage in carcinoma cells MDA-MB-231 post electron irradiation is limited, especially for the case of FLASH irradiation, resulting in less cytosolic cytochrome c but stronger cGAS-STING activation than those in MCF-10A cells. The enhanced difference of cytochrome c leakage between cancer cells and normal cells post FLASH irradiation indicates a potential mechanism of FLASH effect by regulating the apoptotic and inflammatory pathway.

The study of biological effects of high-dose-rate ionizing radiation using animal models remains an urgent problem. In the work, a comparison of proton-induced damage to embryos (the 9th post-fertilization day) and 1-day-old baby chicks (the 18th post-fertilization day) from irradiated eggs of Japanese quail (Coturnix coturnix japonica) irradiated in and outside the Bragg peak with the conventional and ultra-high dose rate D (CONV D < 1 Gy/s, FLASH D [~]100 Gy/s and single-pulse flash - SPLASH D [~]106 Gy/s, respectively) was carried out. The following criteria were used: survival, body weight and body length of embryos, weight of chicks, percentage of erythrocytes with anomalies (with micronuclei, without nuclei, with two nuclei), and the speed of movement of 1-day-old chicks in the open field test. The largest number of dead embryos was recorded after irradiation with 7 and 14 Gy in the plateau region of the proton trajectory. By the criteria of body weight and length, as well as the number of erythrocytes with micronuclei in 9-day-old embryos from eggs irradiated with a dose of 8.5 Gy in the Bragg peak, FLASH and SPLASH modes were found to be the least traumatic compared with the CONV mode. The weight of chicks from eggs irradiated with a dose of 4 Gy in the Bragg peak did not differ from the control and did not depend on the irradiation mode. The lowest death incidence and the smallest number of abnormal erythrocytes were recorded after FLASH and SPLASH irradiation; in chicks that hatched from eggs irradiated in the CONV mode, a tendency for an increase in the number of abnormal erythrocytes was observed. The speed of movement of chicks from FLASH- and SPLASH-irradiated eggs was comparable with that from unirradiated eggs, and chicks from eggs irradiated in the CONV mode were less active than chicks from unirradiated eggs and eggs irradiated in the other regimes. Thus, the irradiation of eggs with a beam of accelerated protons in the Bragg peak in the FLASH/SPLASH modes is less damaging for healthy tissues and for the development of embryos and chicks on the cellular, anatomical, and physiological levels.

Chemotherapy is the primary treatment for patients with acute myeloid leukemia (AML). In addition to factors such as patient age, physical condition, and choice of medication, we have noticed that environmental factors such as altitude may also have a significant impact on post-chemotherapy bone marrow suppression in AML patients in clinical practice. The results indicate that there are differences in the proteomics of the two groups of patients during the bone marrow suppression period after chemotherapy. Differentially expressed proteins are primarily located in the cytoplasm, extracellular space, and nucleus, followed by mitochondria and membranes. These differentially expressed proteins mainly participate in biological processes such as cell and metabolism. For differential protein KEGG pathway enrichment analysis, it was found that metabolic pathways were mainly enriched in the metabolic category, while the PI3K-Akt signaling pathway, HIF-1 signaling pathway, NF-{kappa}B signaling pathway, and calcium signaling pathway were enriched in the signaling pathways.

Three copper(II) complexes containing 1,10-phenanthroline ([CuCl2(phen)]{middle dot}4H2O,1), neocuproine ([CuCl2(neo)]{middle dot}4H2O, 2) and tetramethyl-phenanthroline ([CuCl2(tmp)]{middle dot}4H2O, 3) as the primary ligand and another three copper(II) complexes with the L-Ala-Phe dipeptide as an auxiliary ligand: [Cu(L-Ala-Phe)(phen)]{middle dot}4H2O (4), [Cu(L-Ala-Phe)(neo)]{middle dot}4H2O (5) and [Cu(L-Ala-Phe)(tmp)]{middle dot}4H2O (6), inhibited cell viability in breast cancer MCF-7 cell line, both in the monolayer and spheroid cell culture models. The pair with tetramethyl-phenanthroline displayed a better selectivity index than cisPt and non-cytotoxicity-related ROS induction and apoptosis in the monolayer breast cancer model. Cell proliferation was affected by all compounds in a concentration-dependent manner, with a more substantial effect on the tetramethyl-phenanthroline complexes. Cell viability on multicellular spheroids showed a concentration-dependent reduction from 1 M, with IC50 that were half the one for cisplatin. All copper complexes, except for 1 showed DNA damage, demonstrated by the comet assay at a concentration below the IC50. The role of NHE1 has been linked to many types of cancers. Our study revealed that all compounds inhibited NHE1 activity in MCF-7 cells. However, only complexes containing the dipeptide auxiliary ligand could extend their effect on cell migration (Wound Healing Assay) and MMP-9 activity studied by zimography. Wester Blot analysis showed that expressions of MMP-2, MMP-9, and NHE1 were affected when MCF7 cells were treated with the six compounds as well. Overall, our results reveal an antitumor effect of all copper(II) complexes studied in breast cancer cells and a fundamental role of NHE1 in cell migration.

Lung adenocarcinoma (LUAD), the primary subtype of Non-Small Cell Lung Cancer (NSCLC), accounts for 80% to 85% of cases. Due to suboptimal screening method, LUAD is often detected in late stage, leading to aggressive progression and poor outcomes. Therefore, early disease prognosis for the LUAD is high priority. In order to identify early detection biomarkers, we conducted a meta-analysis of mRNA expression TCGA and GTEx datasets from LUAD patients. A total of 795 differentially expressed genes (DEGs) were identified by exploring the Network-Analyst tool and utilizing combined effect size methods. DEGs refer to genes whose expression levels are significantly different (either higher or lower) compared to their normal baseline expression levels. KEGG pathway enrichment analysis highlighted the TNF signaling pathway as being prominently associated with these DEGs. Subsequently, using the MCODE and CytoHubba plugins in Cytoscape software, we filtered out the top 10 genes. Among these, SOX2 was the only gene exhibiting higher expression, while the others were downregulated. Consequently, our subsequent research focused on SOX2. Further transcription factor-gene network analysis revealed that enhancer of zeste homolog 2 (EZH2) is a significant partner of SOX2, potentially playing a crucial role in euchromatin-heterochromatin dynamics. Structure of SOX2 protein suggest that it is a non-druggable transcription factor, literature survey suggests the same; hence, we drove our focus to investigate on potential drug(s) targeting EZH2. Molecular docking analyses predicted most probable inhibitors of EZH2. We employed several predictive analysis tools and identified GSK343, as a promising inhibitor of EZH2.

An increasing number of scientific papers discuss the promising therapeutic potential of cannabidiol (CBD) not only for the treatment of cancer, but also for asthma and neurodegenerative disorders. This happens mainly due to its proven anticancer, anti-inflammatory, and antioxidant properties. In the field of cancer research, the use of CBD has already been investigated on malignant tumors of the central nervous system, like gliomas. So far, CBD has not yet been explored in the therapy of peripheral nervous system (PNS) tumors. Peripheral nerves reside outside the central nervous system, therefore peripheral nerve tumors can occur anywhere in the body. When the tumor develops within large blood vessels, spinal nerves or involves more than one peripheral nerve, radiotherapy is recommended. Due to high doses of ionizing radiation, complications such as dizziness, damage to adjacent nerves, or malignancy of the lesion may occur. Therefore, it is important to develop a treatment scheme that efficiently reduces tumor volume while maintaining the normal functions of the surrounding cells and decrease the side effects. Herein, we proposed to combine hyperspectral imaging using Raman and FTIR spectroscopy and AFM-IR technique as a novel approach to monitor the therapeutic efficacy of CBD. Performed studies reviled the dual effect of CBD, that protects normal cells from ionizing radiation and increases its toxicity in cancer cells.