Molecular Biology最新文献_第2页

STM2457 is Therapeutic for Idiopathic Pulmonary Fibrosis by Inhibiting the METTL3-CTGF Signaling Axis STM2457通过抑制METTL3-CTGF信号轴治疗特发性肺纤维化

4区生物学

Molecular Biology Pub Date : 2025-07-21 DOI: 10.1134/s0026893325600680

Xin Sun, Jianxing He

引用次数: 1

TRIM56 Mediates Autophagy Inhibition in Esophageal Cancer TRIM56介导食管癌自噬抑制

4区生物学

Molecular Biology Pub Date : 2025-05-11 DOI: 10.1134/s0026893325700232

Jinsheng Gao, Runze Li, Haibao Peng, Sabah Mohammed Al-Harazi, Shanshan Luo, H. M. Hua, Y. Y. Yang, Feiliang Wang, Jiapo Wang

{"title":"TRIM56 Mediates Autophagy Inhibition in Esophageal Cancer","authors":"Jinsheng Gao, Runze Li, Haibao Peng, Sabah Mohammed Al-Harazi, Shanshan Luo, H. M. Hua, Y. Y. Yang, Feiliang Wang, Jiapo Wang","doi":"10.1134/s0026893325700232","DOIUrl":"https://doi.org/10.1134/s0026893325700232","url":null,"abstract":"Tripartite motif containing 56 (TRIM56) has been implicated in tumor development, but its role in esophageal cancer remains unclear. The aim of this study was to determine the correlation between TRIM56 expression and clinicopathological characteristics in esophageal cancer, and investigate the influence of TRIM56 expression on autophagy. Then, we examined TRIM56 expression in esophageal cancer, and TRIM56 expression was upregulated in both esophageal cancer tissues and cells. The upregulated TRIM56 expression was strongly correlated with tumor size, degree of differentiation, and TNM stage. Additionally, Well-differentiated esophageal cancer exhibited TRIM56 upregulation. TRIM56 knockdown upregulated the expression levels of LC3 and ATG12, downregulated the expression of p62, and increased the autophagic flux in Eca109 cells. The findings of this study indicated that TRIM56 inhibits autophagy and that TRIM56 expression is closely related to some clinicopathological characteristics in esophageal cancer. Thus, TRIM56 is a potential novel prognostic biomarker and a promising therapeutic target for esophageal cancer.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"59 4","pages":"598-607"},"PeriodicalIF":0.0,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147898250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Afamin Ameliorates Testosterone Propionate (TP)-Induced Oxidative Stress and Mitochondrial Damage in Human Ovarian Granulosa Tumor Cells (KGN) by Upregulating the Expression of SIRT1 Afamin通过上调SIRT1表达改善人卵巢颗粒肿瘤细胞（KGN）中丙酸睾酮（TP）诱导的氧化应激和线粒体损伤

4区生物学

Molecular Biology Pub Date : 2024-12-01 DOI: 10.1134/s0026893324060074

Ying Che, Zhonghua Li, Zheng Wang, Austin J. Yang

{"title":"Afamin Ameliorates Testosterone Propionate (TP)-Induced Oxidative Stress and Mitochondrial Damage in Human Ovarian Granulosa Tumor Cells (KGN) by Upregulating the Expression of SIRT1","authors":"Ying Che, Zhonghua Li, Zheng Wang, Austin J. Yang","doi":"10.1134/s0026893324060074","DOIUrl":"https://doi.org/10.1134/s0026893324060074","url":null,"abstract":"Abstract Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting women of reproductive age. Considerable research has confirmed that afamin is associated with the prevalence and development of metabolic syndrome. Thus, this study investigated the mechanism of action of afamin in PCOS and its potential therapeutic value. We found that PCOS patients had higher levels of afamin than normal control subjects. Afamin significantly enhanced the overall antioxidant ability and activity of antioxidant enzymes and reduced the levels of 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide anion ( $${text{O}}_{2}^{{centerdot {kern 1pt} - }}$$ ) in human ovarian granulosa tumor cells (KGN cells). In addition, afamin was also found to protect KGN cells against testosterone propionate (TP)-induced mitochondrial damage and apoptosis. Additionally, silencing of SIRT1 revealed that SIRT1 protected KGN cells against TP-induced oxidative stress (OS) injury, mitochondrial damage and apoptosis. Furthermore, this study showed that besides restoring the estrous cycle in PCOS mice, afamin might also reduce the increased cycling testosterone (T) and luteinizing hormone (LH) levels and LH/Follicle-stimulating hormone (FSH) ratio, as well as decrease the number of cystic follicles, indicating the significance of afamin in the treatment of PCOS. Moreover, afamin reduced oxidative damage in PCOS mice by enhancing their antioxidant capacity. Also, afamin may protect KGN cells against TP-induced OS by enhancing their antioxidant ability, restoring mitochondrial function, and inhibiting cell apoptosis by upregulating the expression of SIRT1 . Thus, afamin may play a protective role in PCOS mice.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"58 6","pages":"1250-1267"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1134/S0026893324060074.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

4区生物学

Molecular Biology Pub Date : 2024-12-01 DOI: 10.1134/s0026893324060104

Y. Y. Wang, J. Y. Zhang, Xinhua Zhu, Ying Liu, Xiaogang Wu

引用次数: 1

Development of a New Inhibitor of Bacterial Cystathionine γ-Lyase Based on 6-Bromoindole and Aminothiophene 基于6-溴吲哚和氨基噻吩的细菌半胱硫氨酸γ-裂解酶抑制剂的研制

4区生物学

Molecular Biology Pub Date : 2024-12-01 DOI: 10.1134/s0026893324700584

Роман А. Новиков, Dmitry N. Platonov, Aleksandr Yu. Belyy, Konstantin V. Potapov, Maxim A. Novikov, Yury V. Tomilov, O. I. Kechko, Tatiana A. Seregina, Pavel N. Solyev, Vladimir A. Mitkevich

引用次数: 1

Mechanism of Oxidative Stress Inducing Pyroptosis by Activating the NLRP3/Caspase-1/GSDMD Pathway in Lens Epithelial Cells under High Glucose Environment 高糖环境下氧化应激激活晶状体上皮细胞NLRP3/Caspase-1/GSDMD通路诱导焦亡的机制

4区生物学

Molecular Biology Pub Date : 2024-12-01 DOI: 10.1134/s0026893324060049

Chia-Lang Fang, Lingmei Qian, Nan Ma

{"title":"Mechanism of Oxidative Stress Inducing Pyroptosis by Activating the NLRP3/Caspase-1/GSDMD Pathway in Lens Epithelial Cells under High Glucose Environment","authors":"Chia-Lang Fang, Lingmei Qian, Nan Ma","doi":"10.1134/s0026893324060049","DOIUrl":"https://doi.org/10.1134/s0026893324060049","url":null,"abstract":"Diabetic patients face an increased risk of cataract development. This study investigates the molecular mechanism by which oxidative stress activates the NLRP3/caspase-1/gasdermin-D (GSDMD) pathway, leading to inducing pyroptosis in human lens epithelial cells (HLECs) exposed to high glucose (HG) environments. In vitro, HLECs were cultured in HG medium and treated with N-acetylcysteine (NAC), MCC950 (an NLRP3 inflammasome inhibitor), and VX-765 (a caspase-1 inhibitor). Cell viability was assessed using CCK-8. Reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), lactate dehydrogenase (LDH) levels and activities of superoxide dismutase (SOD) and catalase (CAT) were measured using biochemical kits. Active interleukin (IL)-18 and IL-1β levels in cell culture supernatants were quantified using ELISA kits. Western blot analysis determined levels of GSDMD, GSDMD-N, NLRP3, apoptosis-associated speck-like protein containing CARD (ASC) and cleaved caspase-1. HG induced oxidative stress in HLECs, as indicated by elevated cellular ROS and MDA levels, decreased GSH level, and reduced SOD and CAT activities. HG triggered HLEC pyroptosis, characterized by increased LDH release, levels of cell pyroptosis-related proteins GSDMD-N/GSDMD ratio, and active IL-1β and IL-18 in cell culture supernatants. Inhibition of oxidative stress by NAC partially reversed HG-induced pyroptosis in HLECs. HG induced oxidative stress, activating the NLRP3 inflammasome activation and cleaving caspase-1 cleavage in HLECs. MCC950-suppressed NLRP3 inflammasome activation or VX765-inhibited caspase-1 cleavage partially reversed HG-induced HLEC pyroptosis. Oxidative stress in HLECs under HG conditions induces pyroptosis via the NLRP3/caspase-1/GSDMD pathway.","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"58 6","pages":"1241-1249"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Silencing of the S-Phase Kinase-Associated Protein 2 Gene (SKP2) Inhibits Proliferation and Migration of Hepatocellular Carcinoma Cells 抑制 S 期激酶相关蛋白 2 基因 (SKP2) 可抑制肝细胞癌细胞的增殖和迁移

IF 1.2 4区生物学

Molecular Biology Pub Date : 2024-09-11 DOI: 10.1134/s0026893324700651

Y. Y. Zhao, Z. X. Gao, S. D. Wei, W. Song

{"title":"Silencing of the S-Phase Kinase-Associated Protein 2 Gene (SKP2) Inhibits Proliferation and Migration of Hepatocellular Carcinoma Cells","authors":"Y. Y. Zhao, Z. X. Gao, S. D. Wei, W. Song","doi":"10.1134/s0026893324700651","DOIUrl":"https://doi.org/10.1134/s0026893324700651","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p><i>SKP2</i> gene is an independent prognostic factor in some diseases and a potential oncogene. The molecular mechanism underlying the occurrence and development of hepatoma, and the involvement of the <i>SKP2</i> in this process remain unclear. Here, in order to study the effect of SKP2 on proliferation, apoptosis and migration of hepatoma cells, we utilized lentivirus-mediated RNA interference technology using short hairpin RNAs (shRNAs) specific for <i>SKP2</i>. It was demonstrated that <i>SKP2</i> expression was significantly upregulated in 809 hepatocarcinoma tissues compared to 379 normal liver tissues. The survival time of patients with high levels of SKP2 mRNA was shorter than those with low levels, and <i>SKP2</i> expression was maximal in stage III hepatocellular carcinoma tissues. The effects of <i>SKP2</i> silencing on proliferation, apoptosis, cell cycle, migration, and the expression of apoptosis proteins in Huh7 and HepG2 cells were evaluated by MTT assay, flow cytometry, colony formation assay, Transwell, and Western blot analysis. <i>SKP2</i> expression was significantly reduced in stably transfected Huh7 and HepG2 cells, with knockout efficiencies of 95.7 and 85.8%, respectively. The viability, proliferation, and migration of transfected cancer cells were reduced. In these cells, the apoptosis rate was increased, and the cell cycle was arrested in the G2/M phase. The expression of the apoptosis-associated BCL-2/BAX proteins was decreased, while p53 was upregulated. Thus, we have shown that inhibiting the expression of <i>SKP2</i> can significantly impede cancer cell proliferation and migration, halt the cell cycle, and induce apoptosis.</p>","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"29 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142201113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

New Epigenetic Markers of Age-Dependent Changes in the Cardiovascular System 心血管系统随年龄变化的新表观遗传标记

IF 1.2 4区生物学

Molecular Biology Pub Date : 2024-09-11 DOI: 10.1134/s002689332470064x

L. M. Ermakova, E. A. Davydova, E. V. Kondakova, K. V. Kuchin, M. V. Vedunova

{"title":"New Epigenetic Markers of Age-Dependent Changes in the Cardiovascular System","authors":"L. M. Ermakova, E. A. Davydova, E. V. Kondakova, K. V. Kuchin, M. V. Vedunova","doi":"10.1134/s002689332470064x","DOIUrl":"https://doi.org/10.1134/s002689332470064x","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Cardiovascular diseases remain a predominant global cause of mortality, with a noteworthy rise in the risk of morbidity with advancing age. Besides, it accompanied by a phenomenon of disease rejuvenation in the circulatory system. Currently, epigenetic modifications play a key role in the genesis of cardiovascular diseases (CVD), influencing the complex interaction between genotype and phenotype variability. Consequently, delving into the realm of epigenetic markers offers a promising avenue to unravel the molecular underpinnings of cardiovascular disease pathogenesis. This study endeavors to pinpoint epigenetic markers intricately linked with age-related transformations in the cardiovascular system. The study revealed a robust correlation with age for two cardiological parameters: R wave tension in the augmented left arm lead (RaVL) and carotid-femoral pulse wave velocity (cfPWV). Moreover, these parameters exhibited a strong correlation with the DNA methylation level of 21 CpG-sites (CpGs) examined through the Illumina EPIC array. Notably, the majority of these identified CpG-sites are affiliated with genes involved in the development of pathologies of the cardiovascular system.</p>","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"5 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142201114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Triosephosphate Isomerase Inhibition by Resveratrol: A New Mechanism of Anti-Glycolysis in Breast Cancer 白藜芦醇对磷酸三糖异构酶的抑制：乳腺癌抗糖酵解的新机制

IF 1.2 4区生物学

Molecular Biology Pub Date : 2024-09-11 DOI: 10.1134/s0026893324700663

G. Tuna, O. Akgün, F. Arı

{"title":"Triosephosphate Isomerase Inhibition by Resveratrol: A New Mechanism of Anti-Glycolysis in Breast Cancer","authors":"G. Tuna, O. Akgün, F. Arı","doi":"10.1134/s0026893324700663","DOIUrl":"https://doi.org/10.1134/s0026893324700663","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Breast cancer cells undergo a process of reprogramming their metabolism for rapid growth and proliferation. One of the most common metabolic changes is aerobic glycolysis (Warburg effect), which leads to increased lactate generation and glucose uptake capacity. Triosephosphate isomerase (TPI) is a key enzyme in glycolysis. The effect of Resveratrol (RES), a natural plant compound with known anti-cancer properties, on the TPI enzyme is unknown. The purpose of this study is to examine how RES relates to TPI in breast cancer. TPI levels were examined by ELISA and western-blotting methods in MCF-7 and MDA-MB-231 cells. The changes in lactate dehydrogenase (LDH) activity, methylglyoxal (MGO) formation, nitric oxide synthase (eNOS and iNOS) levels, and MAPK signaling pathway were investigated by colorimetric assays and western-blotting. It was shown for the first time that RES induced a significant decrease in TPI in a dose-dependent manner, with a concomitant increase in levels of MGO, a toxic intermediate. Furthermore, RES treatment decreased LDH activity, and the expression of MAPK, ERK1/2, and JNK, while increasing the expression of eNOS and iNOS levels. The results sign a potential cytotoxic effect of RES due to increased MGO levels resulting from TPI inhibition. The effect of RES on TPI function and glycolysis may be related to NOS induction and the MAPK pathway. These findings are the first data showing the effect of RES treatment on TPI, suggesting that TPI may be a target for energy metabolism in breast cancer.</p>","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":"2 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142200847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Ion Channel Blockers of Influenza A and SARS-CoV-2 Viruses 甲型流感和 SARS-CoV-2 病毒的分子离子通道阻断剂

IF 1.2 4区生物学

Molecular Biology Pub Date : 2024-08-07 DOI: 10.1134/s0026893324700353

Yu. N. Vorobjev

引用次数: 0