DNA and cell biology最新文献

{"title":"Pirfenidone Downregulates eIF6, P311, and TGF-β Expression and Improves Liver Fibrosis Induced by Bile Duct Ligation in Wistar Rats: Evidence for Liver Regeneration.","authors":"Zeynab Yousefi, Mitra Nourbakhsh, Abbas Sahebghadam Lotfi","doi":"10.1089/dna.2024.0194","DOIUrl":"https://doi.org/10.1089/dna.2024.0194","url":null,"abstract":"<p><p>Liver fibrosis (LF) is a clinical disorder characterized by inflammation and excessive accumulation of extracellular matrix (ECM). This study investigates the effects of the antifibrotic compound pirfenidone (PFD) on improving LF through histological changes and modulation of eukaryotic translation initiation factor 6 (eIF6), P311, and transforming growth factor beta (TGF-β) in rats with bile duct ligation (BDL)-induced LF. Rats received daily doses of PFD (200 and 500 mg/kg) for 4 weeks. The study encompassed biochemical, pathological, and immunohistochemical (IHC) analyses. mRNA levels of eIF6, P311, TGF-β, ECM deposition, hepatic stellate cell (HSC) activation, and inflammatory mediator genes were measured by RT-qPCR. Protein levels of eIF6, P311, and TGF-β were detected by western blotting. Compared with the BDL group, PFD dose-dependently reduced hydroxyproline content, liver index, biochemical parameters, fibrosis score, and fibrosis area. PFD also modulated BDL-induced hepatic inflammation, ECM accumulation, and HSC activation. IHC staining of Ki-67 and hepatocyte paraffin-1 revealed that PFD enhanced liver regeneration. The research confirmed that PFD gradually downregulated elevated eIF6, P311, and TGF-β levels in BDL-induced LF. These findings suggest that PFD could be a potential treatment for LF, as it may help attenuate fibrosis and enhance liver regeneration, possibly through the modulation of these specific markers.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142840621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Interplay Between Obesity and Aging in Breast Cancer and Regulatory Function of MicroRNAs in This Pathway.","authors":"Nima Mahdei Nasir Mahalleh, Mina Hemmati, Arezou Biyabani, Fatemeh Pirouz","doi":"10.1089/dna.2024.0170","DOIUrl":"https://doi.org/10.1089/dna.2024.0170","url":null,"abstract":"<p><p>Breast cancer (BC) is a significant contributor to cancer-related deaths in women, and it has complex connections with obesity and aging. This review explores the interaction between obesity and aging in relation to the development and progression of BC, focusing on the controlling role of microRNAs (miRNAs). Obesity, characterized by excess adipose tissue, contributes to a proinflammatory environment and metabolic dysregulation, which are important in tumor development. Aging, associated with cellular senescence and systemic changes, further exacerbates these conditions. miRNAs, small noncoding RNAs that regulate gene expression, play key roles in these processes, impacting pathways involved in cell proliferation, apoptosis, and cancer metastasis, either as tumor suppressors or oncogenes. Importantly, specific miRNAs are implicated in mediating the impact of obesity and aging on BC. Exploring the regulatory networks controlled by miRNAs provides valuable information on new targets for therapy and predictive markers, demonstrating the potential for using miRNA-based interventions to treat BC in obese and elderly individuals. This review emphasizes the importance of integrated research strategies to understand the complex connections between obesity, aging, and miRNA regulation in BC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142804157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Analysis of Autophagy-Related Genes as Diagnostic Markers and Potential Therapeutic Targets for Tuberculosis Through Bioinformatics.","authors":"Tingting Luo, Shijie Shen, Yufei Sun, Saeed El-Ashram, Xia Zhang, Keyu Liu, Chengzhang Cao, Reem Atalla Alajmi, Siqi Deng, Jiangdong Wu, Wanjiang Zhang, Hongying Zhang","doi":"10.1089/dna.2024.0166","DOIUrl":"https://doi.org/10.1089/dna.2024.0166","url":null,"abstract":"<p><p>According to the World Health Organization, <i>Mycobacterium tuberculosis</i> infections affect approximately 25% of the world's population. There is mounting evidence linking autophagy and immunological dysregulation to tuberculosis (TB). As a result, this research set out to discover TB-related autophagy-related biomarkers and prospective treatment targets. We used five autophagy databases to get genes linked to autophagy and Gene Expression Omnibus databases to get genes connected to TB. Then, functional modules associated with autophagy were obtained by analyzing them using weighted gene co-expression network analysis. Both Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were used to examine the autophagy-related genes (ATGs) of important modules. Limma was used to identify differentially expressed ATGs (DE-ATGs), and the external datasets were used to further confirm their identification. We used DE-ATGs and a protein-protein interaction network to search the hub genes. CIBERSORT was used to estimate the kinds and amounts of immune cells. After that, we built a drug-gene interaction network and a network that included messenger RNA, small RNA, and DNA. At last, the differential expression of hub ATGs was confirmed by RT-qPCR, immunohistochemistry, and western blotting. The diagnostic usefulness of hub ATGs was evaluated using receiver operating characteristic curve analysis. Including 508 ATGs, four of the nine modules strongly linked with TB were deemed essential. Interleukin 1B (<i>IL1B</i>), <i>CAPS1</i>, and signal transducer and activator of transcription 1 (<i>STAT1</i>) were identified by intersection out of 22 DE-ATGs discovered by differential expression analysis. Research into immune cell infiltration found that patients with TB had an increased proportion of plasma cells, CD8 T cells, and M0 macrophages. A competitive endogenous RNA network utilized 10 long non-coding RNAs and 2 miRNAs. Then, the <i>IL1B</i>-targeted drug Cankinumad was assessed using this network. During bioinformatics analysis, three hub genes were validated in mouse and macrophage infection models. We found that <i>IL1B</i>, <i>CASP1</i>, and <i>STAT1</i> are important biomarkers for TB. As a result, these crucial hub genes may hold promise as TB treatment targets.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3-Induced m6A Modification Enhances Hsa_Circ_0136959 Expression to Impair the Tumor Characteristics of Papillary Thyroid Carcinoma via Accelerating Ferroptosis.","authors":"Lan Luo, Yanlei Sun, Zongli Cao","doi":"10.1089/dna.2024.0197","DOIUrl":"https://doi.org/10.1089/dna.2024.0197","url":null,"abstract":"<p><p>The number of cases of papillary thyroid cancer (PTC) has gone up significantly in recent years, with high recurrence. Numerous reports have highlighted the participation of circular RNAs (circRNAs) in regulating the advancement of cancers, including PTC. Furthermore, recent studies suggest that N6-methyladenosine (m6A) modified circRNAs play pivotal roles in cancer progression. Hence, we studied the potential role of a novel circRNA, hsa_circ_0136959, and its regulatory mechanism on m6A modification by methyltransferase-like 3 (METTL3) in the tumor characteristics of PTC. The expressions of hsa_circ_0136959 and <i>METTL3</i> were evaluated in PTC samples and cell lines via quantitative real-time polymerase chain reaction. The effect of hsa_circ_0136959 on the malignant properties of PTC was analyzed by performing Cell Counting Kit-8, colony formation, and transwell assays. In addition, its effects on the levels of markers related to ferroptosis (reactive oxygen species, Fe²⁺, and iron) in PTC cells were also assessed. Bioinformatics analysis was done to determine the hsa_circ_0136959 expression and m6A modification sites on it in PTC. The m6A level of hsa_circ_0136959 was analyzed through methylated (m6A) RNA immunoprecipitation. The hsa_circ_0136959 was observed to be downregulated in both PTC samples and cells. <i>In vitro</i> experiments showed that its overexpression impeded the malignant properties of PTC cells. Moreover, hsa_circ_0136959 overexpression increased the levels of ferroptosis-related markers in PTC cells. We also found that <i>METTL3</i> was notably reduced in PTC samples and was positively correlated with hsa_circ_0136959. Mechanistically, METTL3 enhanced hsa_circ_0136959 expression through m6A modification. Our results demonstrate that METTL3-mediated m6A modification elevated hsa_circ_0136959 expression and subsequently restricted the tumor characteristics of PTC by accelerating ferroptosis.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Comprehensive Study on the Distribution of Integrons and Their Gene Cassettes in Clinical Isolates.","authors":"Fatemeh Sarina Abdinia, Kasra Javadi, Mehdi Rajabnia, Elaheh Ferdosi-Shahandashti","doi":"10.1089/dna.2024.0175","DOIUrl":"10.1089/dna.2024.0175","url":null,"abstract":"<p><p>Antibiotic resistance is a significant global health concern, leading to increased morbidity, mortality, and health care costs. Integrons are genetic elements that could acquire and express gene cassettes, including those that confer antibiotic resistance. This comprehensive study focused on the distribution of integrons and their gene cassettes in clinical isolates. This study explored the structure and classification of integrons with particular emphasis on Class I, II, III, and IV integrons. It also discussed the role of integrons in antibiotic resistance. The findings of this study contribute to a better understanding of the mechanisms underlying antibiotic resistance and provide valuable insights for developing strategies to combat this public health crisis.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"579-595"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnesium Lithospermate B Inhibits Colorectal Cancer Cell Progression Through JAK2-STAT3 Signaling.","authors":"Dan Huo, Jinpeng Zhang, Tengfei Ma, Yemao Liu, Jianqing Zhang, Bizhen Dong, Yanjun Lu, Anding Wu, Zhaoxia Jin, Yuping Li","doi":"10.1089/dna.2024.0071","DOIUrl":"10.1089/dna.2024.0071","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second leading cause of cancer death worldwide. The discovery of new effective therapeutic drugs is always a priority. Magnesium lithospermate B (MLB), a native polyphenol acid, is the major component of the aqueous extracts from Danshen, a traditional Chinese medicine derived from the dry root and rhizome of <i>Salvia miltiorrhiza</i>. MLB has been reported to have antioxidant, anti-inflammatory, and ion channel-regulating activities in several diseases, including cardiovascular, renal, and neuronal diseases. However, the effect of MLB on cancer progression has not been reported. In this study, a series of cellular and molecular experiments were conducted on two CRC cell lines (HCT116 and SW480) to investigate the effects of. The results demonstrated that MLB exerted inhibitory effects on cell proliferation, migration, and invasion. The administration of 50 mg/kg MLB inhibited tumor growth in HCT116 cells in xenografted models. Importantly, we found that MLB treatment inhibited the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) signaling pathway, and activation of JAK2-STAT3 signaling with interleukin 6 or overexpression STAT3 significantly suppressed the inhibitory effect of MLB. These findings provide evidence that MLB could inhibit CRC cell progression <i>in vitro</i> and might serve as a potential therapeutic drug for the treatment of CRC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"619-629"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142523909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone Lactylation-Driven GPD2 Mediates M2 Macrophage Polarization to Promote Malignant Transformation of Cervical Cancer Progression.","authors":"Chenlingzi Huang, Lujiadai Xue, Xinzi Lin, Yuan Shen, Xiaoyu Wang","doi":"10.1089/dna.2024.0122","DOIUrl":"10.1089/dna.2024.0122","url":null,"abstract":"<p><p>Cervical cancer (CC) is the most common cancer in women. This study aims to explore the molecular mechanism of lactate secreted by CC cells modulating macrophage polarization in CC via histone lactylation. Normal cervical epithelium (NCE), low-grade squamous intraepithelial lesion (LSIL), high-grade squamous intraepithelial lesion (HSIL), and cervical squamous cell carcinoma (CESC) were collected to assess H3K18la level and macrophage infiltration. Macrophages were incubated with SiHa cell-derived conditioned medium to detect M1 and M2 markers. NCE, HSIL, and CESC samples were used for ChIP-seq of H3K18la. Histone lactylation-dirven <i>GPD2</i> was knocked down in macrophages. Compared to NCE, H3K18la level and M2 macrophage abundance were increased in LSIL, HSIL, and CESC. Lactate secreted by CC cells upregulated H3K18la and M2 markers but downregulated M1 markers in macrophages. ChIP-seq revealed that upregulated pathways in HSIL vs. NCE and CESC vs. HSIL were commonly enriched in lipid metabolism. Notably, lactate upregulated H3K18la-modified <i>GPD2</i> expression in macrophages, and <i>GPD2</i> knockdown reversed lactate induction to M2 macrophages. Collectively, lactate secreted by CC cells upregulates <i>GPD2</i> via histone lactylation, thereby promoting M2 macrophage polarization in CC. This study provides new insights into the role of histone lactylation in macrophage polarization in the malignant transformation of CC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"605-618"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension Control Is Associated with Telomere Length in Older Adults.","authors":"Kenneth Rubio-Carrasco, Paola García de la Torre, José D Martínez-Ezquerro, Sergio Sánchez-García, Elisa García-Vences, Ignacio Camacho-Arroyo, Mauricio Rodríguez-Dorantes, Vanessa González-Covarrubias","doi":"10.1089/dna.2024.0173","DOIUrl":"10.1089/dna.2024.0173","url":null,"abstract":"<p><p>Hypertension is the leading risk for cardiovascular disease and worldwide mortality. Uncontrolled blood pressure worsens with age and its control is part of public health strategies especially for older adults. Telomere length (TL) has been associated with hypertension, with age and sex as relevant confounding factors, but it is not clear whether hypertension control in older adults impacts on TL and if this relationship is consistently age and sex dependent. TL was assessed in leukocytes of 369 hypertensive patients. Individuals were >60 years male (169) and female (200) and have been diagnosed and treated for hypertension for at least four years. TL was measured by RT-PCR using a commercial probe. Regression models were developed considering systolic and diastolic blood pressure control as dependent variables and age, sex, glucose, and lipid levels as confounding factors. TL showed a mean of 7.5 ± 5.1 Kb, and no difference between males and females was observed. We identified a significant association between systolic blood pressure control and TL (<i>p</i> value = 0.039) and a trend for diastolic blood pressure (<i>p</i> value = 0.061). These observations confirm and expand previous reports showing that hypertension control can have an impact on TL and consequently on other factors of healthy aging.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"571-578"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Chondroitin Sulfate Proteoglycan 4 Pseudogene 12 Genetic Variants on Colorectal Cancer Risk: A Case-Control Study.","authors":"Xianlei Zhou, Liwen Guo, Zhenbang Yang, Hongxue Xu, Zhi Zhang, Xuemei Zhang","doi":"10.1089/dna.2024.0174","DOIUrl":"10.1089/dna.2024.0174","url":null,"abstract":"<p><p>This study aims to investigate the correlation between the chondroitin sulfate proteoglycan 4 pseudogene 12 (<i>CSPG4P12</i>) polymorphism and the risk of colorectal cancer (CRC). This case-control study involved 850 patients with CRC and 850 health controls. The genotypes of <i>CSPG4P12</i> (rs2880765, rs6496932, and rs8040855) were determined by the TaqMan-MGB probe method. Logistic regression model was employed to evaluate the association of <i>CSPG4P12</i> single-nucleotide polymorphisms (SNPs) with the risk of CRC by calculating the odds ratio (OR) and 95% confidence interval (CI). The <i>CSPG4P12</i> exhibited lower expression in CRC tissues. Our data showed that the rs6496932 variant increased CRC risk (CA vs. CC: <i>p</i> = 0.006; CA + AA vs. CC: <i>p</i> = 0.005). In contrast, the rs8040855 variant reduced the risk of CRC (CG vs. CC: <i>p</i> < 0.001; CG + GG vs. CC: <i>p</i> < 0.001). Stratification by gender and age revealed that the rs8040855 variant decreased CRC risk; however, the rs6496932 variant increased CRC risk among males (CA vs. CC: <i>p</i> = 0.024; CA + AA vs. CC: <i>p</i> = 0.014) and younger individuals (CA vs. CC: <i>p</i> = 0.004; CA + AA vs. CC: <i>p</i> = 0.010). When stratified by smoking and drinking status, the rs8040855 variant decreased CRC risk among nonsmokers (CG vs. CC: <i>p</i> < 0.001; CG + GG vs. CC: <i>p</i> < 0.001) and nondrinkers (CA vs. CC: <i>p</i> = 0.002; CA + AA vs. CC: <i>p</i> = 0.004). The rs6496932 variant increased CRC risk among nonsmokers (CA vs. CC: <i>p</i> = 0.016; CA + AA vs. CC: <i>p</i> = 0.036) and nondrinkers (CG vs. CC: <i>p</i> < 0.001; CG + GG vs. CC: <i>p</i> < 0.001). Haplotype analysis showed that the <i>CSPG4P12</i> T_rs2880765C_rs6496932G_rs8040855 haplotype reduced the risk of CRC compared with the reference haplotype (<i>CSPG4P12</i> A_rs2880765C_rs6496932C_rs8040855) (OR = 0.46, 95% CI = 0.26-0.82, <i>p</i> = 0.049). These findings highlight the potential of these genetic variants as biomarkers for CRC susceptibility, offering insights into personalized prevention strategies.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"596-604"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SNORA71A Downregulation Enhances Gemcitabine Sensitivity in Gallbladder Cancer Cells by Inducing Ferroptosis Through Inhibiting the AKT/NRF2/GPX4 Pathway.","authors":"Yiyu Qin, Yang Zhou, Hongyan Wu, Haiming Lei, Tingyu Ding, Xinya Shen, Jian Li","doi":"10.1089/dna.2024.0107","DOIUrl":"10.1089/dna.2024.0107","url":null,"abstract":"<p><p>Previous findings have indicated a marked upregulation of SNORA71A in gallbladder cancer (GBC) tissues compared to normal samples. However, the precise role and molecular mechanisms of SNORA71A in GBC remain largely unknown. Moreover, gemcitabine (GEM) drug resistance has been found to lead to unfavorable outcomes and recurrence in GBC patients. Therefore, this study aims to investigate the impact of SNORA71A on GBC and explore its potential effects on the sensitivity of GBC cells to GEM. RT-qPCR was conducted to assess SNORA71A level in matched normal and GBC tissues. Cell proliferation was examined through CCK-8 and 5-ethynyl-2'-deoxyuridine (EdU) assays. Additionally, the expression of proteins in GBC cells was analyzed using western blot assay. The level of SNORA71A was notably higher in GBC tissues relative to normal tissues. SNORA71A overexpression led to increased GBC cell proliferation and invasion. Conversely, SNORA71A deficiency strongly suppressed GBC cell proliferation and invasion and triggered cell apoptosis and ferroptosis. Additionally, downregulation of SNORA71A obviously enhanced the antiproliferative and anti-invasive effects of GEM on GBC cells, whereas these changes were reversed by inhibiting ferroptosis. Furthermore, deficiency of SNORA71A further augmented the GEM-induced downregulation of p-Akt, Nrf2, and GPX4 in NOZ cells; however, these effects were reversed by ferroptosis inhibition. Collectively, these findings suggested that downregulation of SNORA71A may increase the sensitivity of GBC cells to GEM by triggering ferroptosis through inhibiting the AKT/NRF2/GPX4 signaling pathway.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"559-569"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}