Molecular Biology Reports最新文献

Background: Cochlear hair cell senescence is one of the major causes of age-related hearing loss (ARHL) and is significantly related to reactive oxygen species (ROS) accumulation. Research shows that vitamin C (VC) can inhibit ROS accumulation; however, its association with cochlear hair cell senescence remains elusive.

Methods and results: Firstly, a cellular senescence model was established using D-galactose (D-gal) induced HEI-OC1 cells for 24 h. Senescent HEI-OC1 cells were then continued to be treated with the addition of VC or ROS inhibitor (N-acetylcysteine; NAC) for another 24 h, and explored the impact of VC on senescent cochlear hair cell and the potential regulatory mechanisms. The results indicated that D-gal-induced senescent HEI-OC1 cells, manifested as decreased cell viability, increased β-galactosidase activity and p21 protein level, and ROS and pro-inflammatory factors were upregulated, and NF-κB p65 phosphorylation was enhanced. However, the use of VC or NAC can significantly ameliorate these effects and improve HEI-OC1 cell senescence.

Conclusions: This research indicates that VC can ameliorate D-gal-induced senescence of HEI-OC1 cochlear hair cells, and its protective effect may be related to the inhibition of the ROS/NF-κB pathway, which provides a new research direction for the prevention and treatment of ARHL.

Background: Fenugreek (Trigonella foenum-graecum L.) is highly esteemed for its therapeutic properties and is widely used in traditional medicine and modern pharmacology. Enhancing its genetic traits and phytochemical profile, particularly its trigonelline content, can significantly increase its medicinal and agricultural value. This study aims to investigate the effects of gamma rays and Ethyl Methane Sulphonate (EMS) as mutagenic agents on the genetic and phytochemical characteristics of the M2 generation of fenugreek, focusing on genetic diversity and desirable trait enhancement.

Methods and results: To achieve this, various concentrations of EMS and gamma rays were administered to fenugreek seeds, and 27 traits were assessed in the resulting M2 generation. These traits were analyzed for variance, mean values, and correlations. The genetic diversity of 23 M2 offspring was investigated using nine Start Codon Targeted (SCoT) markers. The genetic diversity assessment involved Principal Coordinate Analysis (PCoA) and cluster analysis, utilizing the Dice similarity coefficients and the Unweighted Pair Group Method with Arithmetic Mean (UPGMA). A Bayesian model provided deeper insights into the genetic structure. Results revealed that lower doses of gamma rays (100 Gy) and EMS (0.2%) positively impacted specific traits. In comparison, higher doses (200 Gy and 0.4% EMS) increased seed trigonelline content to 0.71 mg/g dry weight. Among the SCoT markers, SCoT-9 was the most efficient, segregating the populations into three clusters. The first three principal components in the PCoA explained 20% of the total variance, leading to seven subgroup populations distinction.

Conclusions: These findings underscore the potential of induced mutagenesis in enhancing desirable traits in fenugreek.

Prostate cancer is a significant global health concern and one of the leading causes of death from diseases in men. There is a growing interest in exploring new therapeutic approaches to enhance patient treatment outcomes and quality of life. Snake venom-derived compounds have emerged as promising candidates for anticancer treatment due to their potential to be selective and reduce adverse effects. In this article, we conduct a literature review on prostate cancer and discuss the investigation of snake venoms as potential alternatives in treatments to minimize toxicity and maximize efficacy. The potential of snake venom toxins in modulating key processes such as cell apoptosis, inhibition of cell migration, and angiogenesis is highlighted. This comprehensive exploration reaffirms the importance of advancing research into snake venom-based therapies to combat prostate cancer, transform treatment paradigms, and improve the well-being of affected individuals.

Background: Testicular germ cell tumor (TGCT) is a common malignant tumor in adolescents. Now, many long non-coding RNAs (LncRNAs) have been found to have an important function in TGCT. LINC00470 is specifically and highly expressed in TGCT, however, there is still no definite information concerning its role and underlying mechanism in TGCT. The purpose of this research was to look into the involvement of LINC00470 in TGCT and its intrinsic mechanism.

Methods and results: UCSC and GEPIA2 databases were used to analyze the expression of LINC00470, and the BEST website was used to perform GSEA enrichment analysis, immune infiltration analysis, and drug susceptibility analysis. SiRNA transfection was used to silence LINC00470 in TCAM-2 and NCCIT cells. Clone formation and Transwell assays were performed in TGCT cells to confirm the effects of LINC00470 on clone formation, migration, and invasion. Western Blot was performed to determine the expression of proteins related to the EMT and AKT signaling pathways. LINC00470 was specifically highly expressed in TGCT, and played a role in promoting tumor cell clone formation and cell metastasis by affecting the TGF-β and PI3K-AKT-mTOR signaling pathways to regulate the epithelial-mesenchymal transition (EMT) process; LINC00470 may also play a pro-tumor role by negatively regulating immune infiltration; in addition, the expression of LINC00470 was negatively correlated with the chemosensitivity of cisplatin in TGCT patients.

Conclusions: LINC00470 may play a significant role in the etiology and metastasis of TGCT through EMT and AKT-mediated signaling pathways.

Background: Routinely, signs and symptoms of pollinosis worsen during the flowering period of the Cenostigma pluviosum var. peltophoroides (Sibipiruna) trees. This study aimed to determine whether Sibipiruna pollen contains allergenic proteins.

Methods and results: The pollen from mature Sibipiruna anthers was morphologically characterized using optical, scanning electron and emission microscopy. Additionally, biochemical characterization was conducted through Shotgun Label-Free Proteomic Analysis. Three hundred and forty-nine proteins were identified using the UNIPROT database and thirty-six were confirmed as homologous allergenic proteins in the Allergome database.

Conclusions: At the first time, Sibipiruna pollen allergenic proteins have been described and this study provides a deeper understanding of the allergenic proteins present in this pollen. These preliminary findings can be useful to assist in the development of targeted extracts for the study of sensitization and potential immunotherapy in the future.

Glia is pivotal in regulating neuronal stem cell proliferation, functioning, and nervous system homeostasis, significantly influencing neuronal health and disorders. Dysfunction in glial activity is a key factor in the development and progression of brain pathology. However, a deeper understanding of the intricate nature of glial cells and their diverse role in neurological disorders is still required. To this end, we conducted data mining to retrieve literature from PubMed and Google Scholar using the keywords: glia, Drosophila, neurodegeneration, and mammals. The retrieved literature was manually screened and used to comprehensively understand and present the different glial types in Drosophila, i.e., perineurial, subperineurial, cortex, astrocyte-like and ensheathing glia, their relevance with mammalian counterparts, mainly microglia and astrocytes, and their potential to reveal complex neuron-glial molecular networks in managing neurodegenerative processes.

Background: The radiation sensitivity of tumor cells is a critical determinant of their therapeutic response to radiotherapy. Histone deacetylase 6 (HDAC6), beyond its known role in modulating tubulin acetylation and influencing cell motility, is also involved in the DNA damage response, potentially enhancing tumor cell radiosensitivity. Targeted HDAC6 inhibitors have shown substantial promise in preclinical studies aimed at increasing radiosensitivity and inhibiting cellular migration.

Methods: A new HDAC inhibitor, named OXHA, was designed by substituting the phenyl cap of SAHA with an N,5-diphenyloxazole-2-carboxamide group. The inhibitory activity of OXHA was evaluated via in vitro enzymatic assays. Its effects on tumor cell migration and radiosensitization potential were assessed using scratch wound healing assays, micronucleus formation, and clonogenic survival assays.

Result: Enzymatic assays confirmed OXHA's selective inhibition of HDAC6. Compared to SAHA, OXHA significantly increased α-tubulin acetylation while minimally impacting histone H3 acetylation, indicating a high selectivity for HDAC6. In combination with X-ray irradiation, OXHA markedly impaired wound healing in A549 and HepG2 cells, enhanced micronucleus formation, and reduced clonogenic survival across multiple tumor lines.

Conclusion: OXHA exhibits potent and selective HDAC6 inhibition, effectively impeding tumor cell migration and enhancing radiosensitivity across multiple cell lines. These findings suggest that OXHA has strong potential as a therapeutic strategy to improve radiotherapy efficacy.

Background: Esophageal squamous carcinoma (ESCC) is the most prevalent pathological subtype of esophageal cancer (EC). It has the characteristics of significant local invasion, quick disease progression, high recurrence rates, and a dismal prognosis for survival. Phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/AKT) is a signaling system whose aberrant activation regulates downstream factors, leading to the promotion of cancer development. This study looks at a protein called Glycerol-3-phosphate dehydrogenase 1-like (GPD1L), which strongly affects the development of several cancers. However, its association with ESCC development and its underlying mechanisms are not clear.

Methods: In this paper, we analyzed six ESCC transcriptome data obtained from the GEO database. We utilized bioinformatics technology and immunohistochemistry to differentially analyze GPD1L levels of mRNA and protein expression in ESCC and normal adjacent tissues. Furthermore, we conducted survival, co-expression, enrichment, immune infiltration and drug sensitivity analysis. Moreover, we further investigated the role and mechanism of GPD1L by Western Blot (WB), Cell Counting Kit-8 (CCK8), wound healing assay, Transwell assay, and flow cytometry. Finally, the addition of IGF-1, the activator of PI3K/AKT, could rescue the inhibitory effect of GPD1L on ESCC.

Results: The findings manifest that the expression of GPD1L was low in ESCC, and functional experiments showed that GPD1L promoted apoptosis in vitro while blocking cell migration, invasion, and proliferation. Based on mechanism research, GPD1L's impact on ESCC could be explained by its suppression of the PI3K/AKT signaling pathway's activation.

Conclusion: To sum up, our findings imply that GPD1L may impede the initiation and advancement of ESCC via modulating the PI3K/AKT signaling pathway. GPD1L is considered to be a promising therapeutic target and biomarker to diagnose and treat ESCC.

Cerebrovascular disease (CVD) includes a range of conditions affecting the brain's blood vessels, which can result in reduced blood flow to brain tissue. The most common manifestation of CVD is stroke, the second leading cause of death and the third leading cause of disability worldwide. Major risk factors for CVD encompass gender, age, smoking, hypertension, diabetes, physical inactivity, obesity, alcohol consumption, and metabolic syndrome. Research suggests a link between telomere length and an increased risk of CVD, particularly in ischemic stroke cases. This review highlights key findings on the relationship between telomere length and CVD, underscoring its clinical importance. The analysis utilizes scientific literature from PubMed, Scopus, and SciELO up to 2024. Results show that shorter telomere length is associated with various types of CVD, including stroke, ischemic stroke, hemorrhagic stroke, and cardioembolic stroke. Some studies propose that telomere length measurement could be a valuable biomarker for CVD, potentially improving prevention, diagnosis, and management strategies.

Background: Endometriosis is a benign gynecological disease that affects about 1% of all women and up to 15% of women of childbearing age. To date, none of the proposed theories exhaustively explain the pathophysiology of the disease or the associated clinical manifestations. As part of efforts to introduce new methods for the early and non-invasive diagnosis of endometriosis, this project investigated changes in the expression of miR-214-5p and miR-548-5p in ectopic and eutopic tissue compared to normal endometrial tissue.

Materials and methods: Forty-five samples (15 eutopic, 15 ectopic and 15 healthy controls) from women referred to Shahid Sadoughi Hospital (Yazd, Iran). RNA extraction was performed using an RNA extraction kit, and cDNA was synthesized. Two-step qRT-PCR was performed according to the manufacturer's instructions. GraphPad Prism 8 software and Two-Way ANOVA test were used to compare fold-change expression.

Results: The results indicate a significant down-regulation of miR-214-5p expression levels (P-value < 0.05) and an increase in miR-548-5p expression levels (P-value < 0.05) in endometriosis samples compared to those in control tissues.

Conclusion: miR-214-5p and miR-548-5p may regulate the pathogenesis of endometriosis. The down-regulation of miR-214-5p in people with endometriosis compared to healthy individuals may indicate its suppressive role. The upregulation of miR-548-5p could confirm the oncogenic role of this microRNA in endometriosis. The development of new therapeutic strategies targeting these miRNAs could be promising in the treatment of this disease.