The Kaohsiung journal of medical sciences最新文献_第2页

HOXA5 Suppresses NEK7-Mediated Alveolar Epithelial Pyroptosis in Acute Lung Injury by Transcriptionally Inhibiting KAT2A. HOXA5通过转录抑制KAT2A抑制nek7介导的急性肺损伤肺泡上皮焦亡。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-25 DOI: 10.1002/kjm2.70109

Lei Wang, Heng Fan, Qi Wang, Cheng-Jie Jiang, Dan-Hui Li, Ji-Hui Ye

{"title":"HOXA5 Suppresses NEK7-Mediated Alveolar Epithelial Pyroptosis in Acute Lung Injury by Transcriptionally Inhibiting KAT2A.","authors":"Lei Wang, Heng Fan, Qi Wang, Cheng-Jie Jiang, Dan-Hui Li, Ji-Hui Ye","doi":"10.1002/kjm2.70109","DOIUrl":"https://doi.org/10.1002/kjm2.70109","url":null,"abstract":"Alveolar epithelial cell pyroptosis exacerbates inflammation and tissue damage by releasing inflammatory mediators, thereby promoting the development of acute lung injury (ALI). However, the fundamental mechanism underlying alveolar epithelial cell pyroptosis in ALI has not yet been elucidated. Lipopolysaccharide (LPS) was used to simulate ALI in vitro and in vivo. Cell viability was measured using the MTT assay. The expression of these molecules was determined by Western blot, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (RT-qPCR), immunofluorescence, and immunohistochemical assays. The level of pyroptosis was determined using flow cytometry. The interactions between the molecules were validated using co-immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays. Homeobox A5 (HOXA5) was expressed at low levels, whereas lysine acetyltransferase 2A (KAT2A) and NIMA-related kinase 7 (NEK7) were highly expressed in LPS-induced (type II alveolar epithelial) ATII cells and mice. HOXA5 overexpression suppressed pyroptosis in LPS-induced ATII cells and mice. Notably, KAT2A overexpression abolished the effects induced by HOXA5 overexpression in LPS-induced ATII cells. Mechanistically, HOXA5 inhibits KAT2A transcriptional activity by binding to the KAT2A promoter. KAT2A positively regulates NEK7 by promoting H3K9ac/H3K27ac enrichment in the NEK7 promoter. In conclusion, HOXA5 indirectly inhibits NEK7 expression by inhibiting KAT2A transcriptional activity, thereby suppressing pyroptosis in alveolar epithelial cells in ALI.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70109"},"PeriodicalIF":3.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152585","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}

引用次数: 0

Albumin-Bilirubin Score as a Novel Prognostic Prediction Tool for Surgically Treated Head and Neck Squamous Cell Carcinoma. 白蛋白-胆红素评分作为手术治疗头颈部鳞状细胞癌的一种新的预后预测工具。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-25 DOI: 10.1002/kjm2.70115

Ming-Hsien Tsai, Chao-Hui Yang, Yu-Tsai Lin, Hui-Ching Chuang, Tai-Lin Huang, Hui Lu, Wen-Ling Tsai, Chih-Yen Chien, Fu-Min Fang

{"title":"Albumin-Bilirubin Score as a Novel Prognostic Prediction Tool for Surgically Treated Head and Neck Squamous Cell Carcinoma.","authors":"Ming-Hsien Tsai, Chao-Hui Yang, Yu-Tsai Lin, Hui-Ching Chuang, Tai-Lin Huang, Hui Lu, Wen-Ling Tsai, Chih-Yen Chien, Fu-Min Fang","doi":"10.1002/kjm2.70115","DOIUrl":"https://doi.org/10.1002/kjm2.70115","url":null,"abstract":"We investigated the prognostic significance of the preoperative albumin-bilirubin (ALBI) score in surgically treated head and neck squamous cell carcinoma (HNSCC). This retrospective study included 663 patients who underwent radical surgery between 2007 and 2017. The ALBI score, calculated using preoperative bilirubin and albumin levels, was assessed for its impact on overall survival (OS) through univariate and multivariate Cox regression analyses. Patients were randomly assigned to training and validation cohorts in a 3:1 ratio, and using a cutoff of -2.871, patients were stratified into low- and high-ALBI groups, revealing significant prognostic differences in both cohorts. A high preoperative ALBI score was an independent predictor of worse OS in both cohorts, with an ALBI-based nomogram being developed to predict OS with strong concordance indices (0.759 and 0.749 in the training and validation cohorts, respectively). Accordingly, the ALBI score is a simple and effective prognostic marker for improving risk stratification and survival prediction in HNSCC patients.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70115"},"PeriodicalIF":3.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152507","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}

引用次数: 0

Vitexin Attenuates the Growth and Glycolysis of Acute Myeloid Leukemia Cells by Suppressing the HIF-1α-Modulated YAP Pathway Under Hypoxic Conditions. 在缺氧条件下，牡荆素通过抑制hif -1α-调节的YAP通路，减缓急性髓系白血病细胞的生长和糖酵解。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-25 DOI: 10.1002/kjm2.70111

Ping Wang, Jia-Jia Zhang, Fang Zhang, Xiao-Jie Qu, Hui Zhang

{"title":"Vitexin Attenuates the Growth and Glycolysis of Acute Myeloid Leukemia Cells by Suppressing the HIF-1α-Modulated YAP Pathway Under Hypoxic Conditions.","authors":"Ping Wang, Jia-Jia Zhang, Fang Zhang, Xiao-Jie Qu, Hui Zhang","doi":"10.1002/kjm2.70111","DOIUrl":"https://doi.org/10.1002/kjm2.70111","url":null,"abstract":"Vitexin, an apigenin flavone glycoside, exhibits antitumor activity against various cancers including leukemia. Hypoxia enhances glycolysis, thereby promoting tumor growth. In this study, we aimed to explore the effects of vitexin on hypoxia-induced growth and glycolysis in acute myeloid leukemia (AML) cells and determine the underlying molecular mechanisms. Our findings showed that vitexin inhibited the hypoxia-induced increase in viability and proliferation of AML cells. Vitexin suppressed glucose uptake, lactate production, and the expression of hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase A in hypoxia-exposed AML cells. Vitexin also blocked the hypoxia-induced increase in hypoxia-inducible factor 1α (HIF-1α) and Yes-associated protein (YAP) expression, as well as the decrease in p-YAP expression. In addition, our results demonstrate that the YAP pathway is regulated by HIF-1α in hypoxia-exposed AML cells and participates in the inhibitory effects of vitexin on hypoxia-induced AML cell growth and glycolysis. These results indicate that vitexin prevents hypoxia-induced growth and glycolysis in AML cells by regulating the HIF-1α/YAP signaling pathway.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70111"},"PeriodicalIF":3.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152554","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}

引用次数: 0

Clinical Outcomes of Different Generation EGFR TKIs in Susceptible EGFR-Mutated Advanced Nonsmall-Cell Lung Cancer. 不同代EGFR TKIs在易感EGFR突变晚期非小细胞肺癌中的临床结果

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-25 DOI: 10.1002/kjm2.70105

Chia-Yu Kuo, Tien-Chi Huang, Chih-Jen Yang, Mei-Hsuan Lee, Jui-Ying Lee, Ying-Ming Tsai, Kuan-Li Wu, Cheng-Hao Chuang, Inn-Wen Chong, Jen-Yu Hung

{"title":"Clinical Outcomes of Different Generation EGFR TKIs in Susceptible EGFR-Mutated Advanced Nonsmall-Cell Lung Cancer.","authors":"Chia-Yu Kuo, Tien-Chi Huang, Chih-Jen Yang, Mei-Hsuan Lee, Jui-Ying Lee, Ying-Ming Tsai, Kuan-Li Wu, Cheng-Hao Chuang, Inn-Wen Chong, Jen-Yu Hung","doi":"10.1002/kjm2.70105","DOIUrl":"https://doi.org/10.1002/kjm2.70105","url":null,"abstract":"Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are indicated for advanced lung adenocarcinoma patients harboring susceptible EGFR mutations. The aim of this retrospective study was to compare the effectiveness of different generations of EGFR TKIs. We enrolled 421 patients with stage IV lung adenocarcinoma and sensitizing EGFR mutations receiving an EGFR-TKI as their first-line therapy, including first-generation (1st G, gefitinib and erlotinib), second-generation (2nd G, afatinib), and third-generation (3rd G, osimertinib) EGFR TKIs. The median progression free survival (PFS) (12.10 vs. 16.67 months vs. not reached; p = 0.0002) and overall survival (OS) (31.23 vs. 45.97 months vs. not reached; p = 0.0215) were significantly different between different generations of EGFR TKIs. 3rd G EGFR TKI provided the best PFS, particularly in patients with exon 19 deletion. The patients receiving 1st G EGFR TKIs (p = 0.005), with exon 19 deletion (p = 0.001) and PFS ≥ 270 days (p = 0.012) had a significantly higher T790M mutation rate. There was no survival difference between the patients receiving frontline 3rd G EGFR TKI and those receiving 3rd G EGFR TKI as sequential therapy (median OS 46.60 months vs. not reached, p = 0.1941). The OS of the patients who did not receive 3rd G EGFR TKI as sequential therapy was significantly worse than those receiving 3rd G EGFR TKI as first-line therapy (median OS 22.47 months vs. not reached, p = 0.0042). In conclusion, 3rd G EGFR TKI may provide better survival benefits as first-line therapy for patients harboring sensitizing EGFR mutations, particularly those with exon 19 deletion.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70105"},"PeriodicalIF":3.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152595","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}

引用次数: 0

Regulatory Effect and Mechanism of Tanshinone I on Cell Apoptosis in Steroid-Induced Osteonecrosis of the Femoral Head. 丹参酮I对激素性股骨头坏死细胞凋亡的调控作用及机制。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-18 DOI: 10.1002/kjm2.70086

Qing Su, Jia Chen

{"title":"Regulatory Effect and Mechanism of Tanshinone I on Cell Apoptosis in Steroid-Induced Osteonecrosis of the Femoral Head.","authors":"Qing Su, Jia Chen","doi":"10.1002/kjm2.70086","DOIUrl":"https://doi.org/10.1002/kjm2.70086","url":null,"abstract":"Steroid-induced osteonecrosis of the femoral head (SIONFH) is a debilitating orthopedic condition. This study investigated the mechanism of Tanshinone I (TsI) in SIONFH modulating apoptosis in SIONFH via the PI3K/AKT/mTOR pathway. A SIONFH rat model was treated with TsI and a PI3K activator. Bone mineral density (BMD), bone volume/total volume (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), and trabecular separation (Tb.Sp) were determined by microCT. Empty lacunae count, Osteopontin, and apoptosis of the femoral head tissues were assessed. Levels of Bax, cleaved-caspase-3, Bcl-2, and AKT, PI3K, and mTOR phosphorylation in femoral head tissues were determined by Western blot. SIONFH rats exhibited decreased BMD, BV/TV, Tb.N, and Tb.Th, increased Tb.Sp, reduced Osteopontin-positive cells, increased empty lacunae rate, and TUNEL and Osteopontin co-positive cells, elevated Bax and cleaved-caspase-3 protein levels, and diminished Bcl-2 protein expression. TsI promoted osteogenesis, attenuated SIONFH, and reduced apoptosis in SIONFH rats. TsI inhibited AKT, PI3K, and mTOR phosphorylation levels in the femoral head tissues of SIONFH rats, thereby repressing the PI3K/AKT/mTOR pathway activation. Activating the PI3K/AKT/mTOR pathway partially reversed TsI's effect in rats. Collectively, TsI limited the PI3K/AKT/mTOR pathway activation to reduce osteocyte apoptosis in SIONFH rats, which provided potential therapeutic insights for SIONFH treatment.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70086"},"PeriodicalIF":3.1,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145088224","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}

引用次数: 0

GLIS2 Promotes Epithelial-Mesenchymal Transition and Gastric Cancer Progression by Regulating BGN to Activate the Wnt/β-Catenin Pathway. GLIS2通过调节BGN激活Wnt/β-Catenin通路促进上皮-间质转化和胃癌进展。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-12 DOI: 10.1002/kjm2.70103

Juan Yan, Ya-Peng Deng

引用次数: 0

Glutamate Exacerbates Traumatic Brain Injury-Induced Acute Lung Injury Through NMDAR/ROS/Ca²⁺ Signaling Pathway in Pulmonary Endothelial Cells. 谷氨酸通过肺内皮细胞NMDAR/ROS/Ca2+信号通路加重外伤性脑损伤诱导的急性肺损伤

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-10 DOI: 10.1002/kjm2.70087

Song Zhou, Ying-Ying Lou, Xue-Zhen Ying

{"title":"Glutamate Exacerbates Traumatic Brain Injury-Induced Acute Lung Injury Through NMDAR/ROS/Ca2+ Signaling Pathway in Pulmonary Endothelial Cells.","authors":"Song Zhou, Ying-Ying Lou, Xue-Zhen Ying","doi":"10.1002/kjm2.70087","DOIUrl":"https://doi.org/10.1002/kjm2.70087","url":null,"abstract":"Traumatic brain injury (TBI) causes a high level of blood glutamate, which triggers host defense by activating oxidative stress and inflammation response. However, the concrete mechanism underlying its exacerbating effects on acute lung injury (ALI) severity remains unknown. In the present study, we aim to demonstrate the special role of N-methyl-D-aspartate receptor (NMDAR) in regulating glutamate-related inflammation signaling to facilitate the sustaining injury. After the interventions, blood glutamate concentration was measured using HPLC-MS/MS. The level of pro-inflammation cytokines, wet/dry weight ratio, protein concentration, and lung injury score were measured to examine the severity of lung damage. The oxidative status was evaluated by measuring the levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) activity, and intracellular Ca2+ concentration. Endothelial cell dysfunction was assessed through dye extravasation assay and quantification of p-NFAT, p-p65, ICAM-1, and VCAM-1 expression levels. Results showed that glutamate activated the NMDAR pathway, inducing endothelial barrier dysfunction via ROS/MDA elevation and SOD suppression. This cascade promoted the concentration of Ca2+, activating both nuclear factor of activated T cells (NFAT) and nuclear factor kappa-B (NF-κB) pathway. Glutamate administration exacerbated NMDAR activation, leading to persistent lung injury following TBI. Memantine-mediated NMDAR blockade effectively attenuated this injury. Our findings indicate that blood glutamate elevation may trigger TBI-associated acute lung injury (TBI-ALI) through endothelial NMDAR/ROS/Ca2+ signaling.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70087"},"PeriodicalIF":3.1,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031628","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}

引用次数: 0

The Proteomic Profiling of Circulating Extracellular Vesicles of Western Diet and Chemical-Induced Murine MASH Model. 西方饮食和化学诱导小鼠MASH模型循环细胞外囊泡的蛋白质组学分析。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-09 DOI: 10.1002/kjm2.70107

Szu-Jen Wang, Yung-Ho Wang, Jee-Fu Huang, En-Sheng Lin, Wei-Shiun Chen, Chia-Yang Li, Chia-Yen Dai, Wan-Long Chuang, Ming-Lung Yu, Shu-Chi Wang

{"title":"The Proteomic Profiling of Circulating Extracellular Vesicles of Western Diet and Chemical-Induced Murine MASH Model.","authors":"Szu-Jen Wang, Yung-Ho Wang, Jee-Fu Huang, En-Sheng Lin, Wei-Shiun Chen, Chia-Yang Li, Chia-Yen Dai, Wan-Long Chuang, Ming-Lung Yu, Shu-Chi Wang","doi":"10.1002/kjm2.70107","DOIUrl":"https://doi.org/10.1002/kjm2.70107","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly prevalent chronic liver condition that can progress to severe complications such as metabolic dysfunction-associated steatohepatitis (MASH). Despite its growing burden, there are no reliable non-invasive biomarkers for tracking disease progression. In this study, we established a murine MASLD/MASH model using a high-fat diet and chemical (CCl4) induction. We analyzed serum-derived extracellular vesicles (EVs) at 14 and 28 weeks to identify stage-specific proteomic signatures. Proteomic profiling of circulating EVs revealed key proteins associated with disease progression, including cathepsin B (Ctsb) and prosaposin (Psap) in early MASLD, and coagulation factor XIII A chain (F13a1) and polymeric immunoglobulin receptor (Pigr) in early MASH. The significant and severe MASH stages notably enriched Psma2, Psmb3, and Psmb5. These findings suggest EV-associated proteins may be promising non-invasive biomarkers for differentiating MASLD/MASH stages and guiding clinical monitoring.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70107"},"PeriodicalIF":3.1,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145025061","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}

引用次数: 0

RBM15 Mediated m6A Modification of SRSF1 Inhibits Cuproptosis in Non-Small Cell Lung Cancer by Mediating ATP7B Alternative Splicing. RBM15介导的m6A修饰SRSF1通过介导ATP7B选择性剪接抑制非小细胞肺癌铜细胞增生。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-09 DOI: 10.1002/kjm2.70098

Shan-Shan Mao, Dong-Yu Wu, Rong-Hua Cui, Xiao-Zhen Cheng

{"title":"RBM15 Mediated m6A Modification of SRSF1 Inhibits Cuproptosis in Non-Small Cell Lung Cancer by Mediating ATP7B Alternative Splicing.","authors":"Shan-Shan Mao, Dong-Yu Wu, Rong-Hua Cui, Xiao-Zhen Cheng","doi":"10.1002/kjm2.70098","DOIUrl":"https://doi.org/10.1002/kjm2.70098","url":null,"abstract":"Inhibition of cuproptosis contributes to the development of non-small cell lung cancer (NSCLC). The expression of RNA-binding motif protein 15 (RBM15) is upregulated in NSCLC. Nonetheless, its relationship with cuproptosis remains unclear. This study aimed to explore the role of RBM15 in regulating cuproptosis in NSCLC. A549 cells were treated with elesclomol (ES-Cu) and tetrathiomolybdate (TTM) to induce or inhibit cellular cuproptosis. EdU, CCK-8, Transwell assays, and flow cytometry were used to detect cellular phenotypes. The expression levels of relevant genes and proteins were analyzed using RT-qPCR and western blotting. RIP and MeRIP were utilized to investigate the interaction of RBM15 and YT521-B homology domain family-3 (YTHDF3) with serine/arginine splicing factor 1 (SRSF1). The effect of the RBM15/m6A/SRSF1/ATP7B axis on tumor growth was evaluated using tumor xenografts in nude mice. Copper levels were assessed using commercially available kits. In NSCLC cells, RBM15 suppression inhibited proliferation and invasion while promoting cuproptosis; however, treatment with TTM (copper chelators) reversed the effect of sh-RBM15. ES-Cu treatment inhibited cell proliferation and invasion, and RBM15 knockdown further promoted the effect of ES-Cu, but upregulated RBM15 reversed the regulatory effect of ES-Cu. Mechanistically, RBM15 promoted the m6A modification of SRSF1 by recruiting YTHDF3. Increased SRSF1 enhanced ATPase copper-transporting beta (ATP7B) exon 21 splicing. Furthermore, SRSF1 promoted cell proliferation and invasion and inhibited cuproptosis by regulating ATP7B alternative splicing. Finally, we verified that RBM15 promoted tumor growth by mediating SRSF1 in vivo. In short, RBM15-mediated m6A modification enhanced SRSF1 stability, and SRSF1 promoted ATP7B alternative splicing to inhibit cuproptosis, thereby promoting NSCLC cell proliferation and tumor growth.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70098"},"PeriodicalIF":3.1,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145025096","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}

引用次数: 0

Rosuvastatin Upregulates RCOR1 to Repress C10ORF10 Transcription and Alleviate Oxidative Stress and Plaque Formation in Atherosclerosis. 瑞舒伐他汀上调RCOR1抑制C10ORF10转录，缓解动脉粥样硬化中氧化应激和斑块形成

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2025-09-09 DOI: 10.1002/kjm2.70106

Xin Fu, Chuang Liu, Ya-Li Chen, Jie-Lin Qin, Ting-Ting Wang, Shan-Shan Fu

{"title":"Rosuvastatin Upregulates RCOR1 to Repress C10ORF10 Transcription and Alleviate Oxidative Stress and Plaque Formation in Atherosclerosis.","authors":"Xin Fu, Chuang Liu, Ya-Li Chen, Jie-Lin Qin, Ting-Ting Wang, Shan-Shan Fu","doi":"10.1002/kjm2.70106","DOIUrl":"https://doi.org/10.1002/kjm2.70106","url":null,"abstract":"Rosuvastatin (RVS) is an HMG-CoA reductase inhibitor with lipid-lowering properties. This study aims to investigate the role of RVS in plaque formation in atherosclerosis (AS) and its functional mechanism. ApoE-/- mice were fed a high-fat diet to generate a mouse model of AS. RVS treatment reduced serum levels of total cholesterol, triglycerides, and low-density lipoprotein cholesterol in atherosclerotic mice, alleviated oxidative stress, and ameliorated lipid deposition, plaque formation, and fibrosis in the mouse aortic tissues. In vitro, it reduced reactive oxygen species and suppressed the proliferation and migration of oxidized low-density lipoprotein-challenged human vascular smooth muscle cells (HVSMCs). REST corepressor 1 (RCOR1) was identified as a target protein upregulated by RVS. It was found to repress transcription of decidual protein induced by progesterone 1 (DEPP1/C10ORF10) by binding to its promoter. Silencing of RCOR1 negated the AS-ameliorating effects of RVS in mice and HVSMCs. However, the AS-like symptoms in mice and HVSMC activity were suppressed by the additional C10ORF10 silencing. In conclusion, this study demonstrates that RVS alleviates oxidative stress and reduces atherosclerotic plaque formation by increasing RCOR1-mediated transcriptional repression of C10ORF10.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70106"},"PeriodicalIF":3.1,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145025018","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}

引用次数: 0