Kaohsiung Journal of Medical Sciences最新文献_第7页

KLF9 inhibits the proliferation, invasion, and migration of renal cell carcinoma through the SDF-1/CXCR4 axis. KLF9通过SDF-1/CXCR4轴抑制肾细胞癌的增殖、侵袭和迁移。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 DOI: 10.1002/kjm2.12671

Peng Yu, Long Cheng, Wei-Mu Xia, Ding-Yi Liu, Jia-Shun Yu, Yan-Feng Zhou, Yong-Jun Zheng

{"title":"KLF9 inhibits the proliferation, invasion, and migration of renal cell carcinoma through the SDF-1/CXCR4 axis.","authors":"Peng Yu, Long Cheng, Wei-Mu Xia, Ding-Yi Liu, Jia-Shun Yu, Yan-Feng Zhou, Yong-Jun Zheng","doi":"10.1002/kjm2.12671","DOIUrl":"https://doi.org/10.1002/kjm2.12671","url":null,"abstract":"Altered Krüppel-like factor 9 (KLF9) expression can regulate the progression of several cancers, including renal cell carcinoma (RCC). This study was conducted to investigate the role of KLF9 in the proliferation, invasion, and migration of RCC cells via regulation of stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4). The expression patterns of KLF9, SDF-1, and CXCR4 in the experimental cell lines were determined by real-time quantitative polymerase chain reaction and Western blotting. After transfection of the KLF9 siRNA and KLF9 pcDNA, cell proliferation, invasion, and migration were evaluated by experiments including cell counting kit-8, colony formation, and Transwell assays. The binding of KLF9 to the SDF-1 promoter was analyzed by chromatin immunoprecipitation and dual-luciferase assay. The rescue experiment was performed using the recombinant SDF-1 protein and KLF9 pcDNA. KLF9 was downregulated in the RCC cells. KLF9 knockdown induced the proliferation, invasion, and migration of RCC cells, whereas KLF9 overexpression elicited the opposite roles. Mechanically, KLF9 bound to the SDF-1 promoter, repressed SDF-1 transcription, and reduced the SDF-1/CXCR4 expression levels. Activation of the SDF-1/CXCR4 axis attenuated the inhibitory role of KLF9 overexpression in RCC cell growth. Ordinarily, KLF9 suppressed the proliferation, invasion, and migration of RCC cells by repressing the SDF-1/CXCR4 signaling.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 6","pages":"587-595"},"PeriodicalIF":3.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9659061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Caffeic acid phenethyl ester reverses doxorubicin resistance in breast cancer cells via lipid metabolism regulation at least partly by suppressing the Akt/mTOR/SREBP1 pathway. 咖啡酸苯乙酯通过脂质代谢调节逆转乳腺癌细胞的阿霉素耐药，至少部分通过抑制Akt/mTOR/SREBP1通路。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 DOI: 10.1002/kjm2.12675

Lu-Chang Liang, Lei Zhao, Bo Yu, Han-Xiang Hu, Xu-Hua He, Yan-Min Zhang

{"title":"Caffeic acid phenethyl ester reverses doxorubicin resistance in breast cancer cells via lipid metabolism regulation at least partly by suppressing the Akt/mTOR/SREBP1 pathway.","authors":"Lu-Chang Liang, Lei Zhao, Bo Yu, Han-Xiang Hu, Xu-Hua He, Yan-Min Zhang","doi":"10.1002/kjm2.12675","DOIUrl":"https://doi.org/10.1002/kjm2.12675","url":null,"abstract":"Chemotherapy is one of the common treatment methods for breast cancer, but chemoresistance is a severe challenge. Caffeic acid phenethyl ester (CAPE) is an active ingredient of propolis extract and has been shown to have a variety of beneficial effects, and its potential as a treatment for breast cancer is worth exploring. The effects of CAPE on doxorubicin (DOX) resistance were determined by cell counting kit-8 (CCK-8) assay, colony-formation assay, and flow cytometry. Oil Red O staining and the detection of free fatty acids, triglycerides, phospholipids, and cholesterol were performed to assess the status of lipid metabolism. Quantitative polymerase chain reaction (qPCR) and western blotting were applied to investigate the molecules involved in lipid metabolism and the protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/sterol regulatory element binding protein 1 (SREBP1) pathway. CAPE treatment reversed DOX resistance in breast cancer cells and suppressed their lipid metabolism. In addition, CAPE combined with DOX remarkably suppressed SREBP1 expression in part by inhibiting Akt/mTOR pathway activation. Furthermore, by inhibiting lipid metabolism, partly via the Akt/mTOR/SREBP1 pathway, CAPE ultimately reversed DOX resistance in breast cancer. Our results suggest that CAPE treatment reversed DOX resistance in breast cancer cells, at least in part by inhibiting Akt/mTOR/SREBP1 pathway-mediated lipid metabolism, indicating that CAPE may be an effective substance to assist in the treatment of breast cancer.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 6","pages":"605-615"},"PeriodicalIF":3.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9977034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

The identification and phylogenetic analysis of SARS-CoV-2 delta variants in Taiwan. 台湾地区SARS-CoV-2 δ型病毒的鉴定及系统发育分析。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 DOI: 10.1002/kjm2.12665

Li-Teh Liu, Jih-Jin Tsai, Justin Jang Hann Chu, Chun-Hong Chen, Liang-Jen Chen, Ping-Chang Lin, Ching-Yi Tsai, Miao-Chen Hsu, Wan-Long Chuang, Shang-Jyh Hwang, Inn-Wen Chong

{"title":"The identification and phylogenetic analysis of SARS-CoV-2 delta variants in Taiwan.","authors":"Li-Teh Liu, Jih-Jin Tsai, Justin Jang Hann Chu, Chun-Hong Chen, Liang-Jen Chen, Ping-Chang Lin, Ching-Yi Tsai, Miao-Chen Hsu, Wan-Long Chuang, Shang-Jyh Hwang, Inn-Wen Chong","doi":"10.1002/kjm2.12665","DOIUrl":"https://doi.org/10.1002/kjm2.12665","url":null,"abstract":"In Taiwan, coronavirus disease 2019 (COVID‐19) involving the delta variant occurred after that involving the alpha variant in 2021. In this study, we aimed to analyze the Delta variant. A total of 318 patients in Taiwan infected with delta variants were identified. The case fatality rate (CFR) of patients infected with delta variants was 0.94% in Taiwan compared with that of those infected with alpha variants (5.95%). The possible reasons for the low CFR might be hybrid immunity due to infection and rapid promotion of the COVID‐19 vaccination program during the alpha variant outbreak. We identified three 21J delta variants. Two long gene deletions were detected in these severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) isolates: ORF7aΔ91 in KMUH‐8 and SpikeΔ30 in KMUH‐9. Protein structure prediction indicates that ORF7aΔ91 results in malfunction of NS7a as an interferon antagonist and that SpikeΔ30 results in a truncated spike protein (N679–A688del), resulting in a lower infection rate compared with the delta variant without these deletions. The impact of these two deletions on SARS‐CoV‐2‐associated pathogenesis deserves further investigation. Delta variants still exist in many regions in the omicron era, and the backbone of the delta variant genome possibly spread worldwide in the form of delta‐omicron hybrids (deltacron; e.g., XBC.1 and XAY.2), which casts a potential threat to public health. Our study further highlighted the importance of more understanding of the delta variants.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 6","pages":"624-636"},"PeriodicalIF":3.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9605253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Expression level of serum miR-374a-5p in patients with acute pancreatitis and its effect on viability, apoptosis, and inflammatory factors of pancreatic acinar cells induced by cerulein. 急性胰腺炎患者血清miR-374a-5p的表达水平及其对蓝蛋白诱导胰腺腺泡细胞活力、凋亡及炎症因子的影响

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 DOI: 10.1002/kjm2.12666

Fu-Jun Wang, Xue Mei

{"title":"Expression level of serum miR-374a-5p in patients with acute pancreatitis and its effect on viability, apoptosis, and inflammatory factors of pancreatic acinar cells induced by cerulein.","authors":"Fu-Jun Wang, Xue Mei","doi":"10.1002/kjm2.12666","DOIUrl":"https://doi.org/10.1002/kjm2.12666","url":null,"abstract":"Acute pancreatitis (AP) is one of the life-threatening diseases of the digestive system. MicroRNA has been asserted to be a regulator of AP. This paper explored the miR-374a-5p expression in AP patients and investigated the efficacy of AR42J cells. In this study, 60 healthy people, 58 MAP patients and 58 SAP patients were included, and the serum miR-374a-5p levels of the subjects were detected by RT-qPCR technology. The pancreatitis cell model was structured by stimulating AR42J cells with cerulein. Next, cell viability and apoptosis were detected by CCK-8 assay and flow cytometry. ELISA was used to measure the concentration of cytokines, such as TNF-α, IL-6, and IL-1β. The data showed that miR-374a-5p was downregulated in samples from AP patients, while showing discriminative power for AP populations. Attenuated miR-374a-5p were negatively bound up with patients' Ranson score and APACHE II score. Besides, miR-374a-5p was declined in cerulein-treated AR42J cells and forced elevation of miR-374a-5p was beneficial to increase cell viability, and inhibit cell apoptosis and inflammation. The present study found that miR-374a-5p was reduced in AP serum samples, and up-regulated expression level of miR-374a-5p in cell models had a protective effect on cerulein-induced inhibition of cell function and inflammatory response.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 6","pages":"616-623"},"PeriodicalIF":3.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9977005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nonbacterial thrombotic endocarditis as a paraneoplastic manifestation of newly diagnosed splenic large B cell lymphoma. 非细菌性血栓性心内膜炎作为新诊断的脾大B细胞淋巴瘤的副肿瘤表现。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 Epub Date: 2023-03-23 DOI: 10.1002/kjm2.12677

Ching-Yun Wang, Hsiang-Chun Lee, Ren-Jie Lin, Jih-Jin Tsai

引用次数: 1

Optical coherence tomography biomarkers for myopic choroidal neovascularization treated with anti-vascular endothelial growth factor. 抗血管内皮生长因子治疗近视脉络膜新生血管的光学相干断层扫描生物标志物研究。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 DOI: 10.1002/kjm2.12669

Daniel Yu Lee, Po-Ying Wu, Shwu-Jiuan Sheu

{"title":"Optical coherence tomography biomarkers for myopic choroidal neovascularization treated with anti-vascular endothelial growth factor.","authors":"Daniel Yu Lee, Po-Ying Wu, Shwu-Jiuan Sheu","doi":"10.1002/kjm2.12669","DOIUrl":"https://doi.org/10.1002/kjm2.12669","url":null,"abstract":"In recent years, optical coherence tomography (OCT) biomarkers for specific retinal diseases have been found to be associated with treatment outcome and disease recurrence. The main purposes of this study were to identify OCT biomarkers for myopic choroidal neovascularization (mCNV) treated with intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF). OCT features in 43 eyes of 39 patients with mCNV treated with anti-VEGF with at least 1 year of follow-up were retrospectively analyzed. Eyes with subretinal hyperreflective material (SHM) in baseline spectral-domain OCT (SD-OCT) had significantly more visual improvement than eyes without SHM at month 6 (p = 0.007) and had a trend of more visual improvement than eyes without SHM (p = 0.058) at month 12. Eyes with subretinal fluid (SRF) at baseline had significantly more central retinal thickness (CRT) decrease than patients without SRF at month 6 and 12 (p = 0.012 and 0.006 respectively). In univariate regression analysis, dome-shaped macula (DSM), SRF in baseline OCT image and fuzzy border of mCNV when entering pro re nata (PRN) injection protocol tended to have higher risk of disease recurrence in 1 year (odds ratio: 14.86 (p = 0.003), 3.75 (p = 0.049) and 22.92 (p < 0.001) respectively). However, they were not significant in multivariate regression analysis. OCT biomarkers at baseline could provide prognostic information for mCNV management.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 6","pages":"637-643"},"PeriodicalIF":3.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9607810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Exosomal miR-196a-5p enhances radioresistance in lung cancer cells by downregulating NFKBIA. 外泌体miR-196a-5p通过下调NFKBIA增强肺癌细胞的放射耐药。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 DOI: 10.1002/kjm2.12673

Fei Yao, Wei Shi, Fang Fang, Meng-Yu Lv, Mei Xu, Shan-Yan Wu, Chun-Li Huang

{"title":"Exosomal miR-196a-5p enhances radioresistance in lung cancer cells by downregulating NFKBIA.","authors":"Fei Yao, Wei Shi, Fang Fang, Meng-Yu Lv, Mei Xu, Shan-Yan Wu, Chun-Li Huang","doi":"10.1002/kjm2.12673","DOIUrl":"https://doi.org/10.1002/kjm2.12673","url":null,"abstract":"Radiation therapy is recognized as an effective modality in the treatment of lung cancer, but radioresistance resulting from prolonged treatment reduces the chances of recovery. MicroRNAs (miRNAs) play a pivotal role in radiotherapy immunity. In this study, we aimed to investigate the mechanism by which miR-196a-5p affects radioresistance in lung cancer. The radioresistant lung cancer cell line A549R26-1 was established by radiation treatment. Cancer-associated fibroblasts (CAFs) and normal fibroblasts (NFs) were observed by microscopy, and the expression levels of CAF-specific marker proteins were detected by immunofluorescence. The shape of the exosomes was observed by electron microscopy. A CCK-8 assay was used to detect cell viability, while clone formation assays were used to detect cell proliferative capacity. Flow cytometry was performed to investigate apoptosis. The binding of miR-196a-5p and NFKBIA was predicted and further verified by the dual luciferase reporter experiment. qRT-PCR and western blotting were used to detect gene mRNA and protein levels. We found that exosomes secreted by CAFs could enhance lung cancer cell radioresistance. Moreover, miR-196a-5p potentially bound to NFKBIA, promoting malignant phenotypes in radioresistant cells. Furthermore, exosomal miR-196a-5p derived from CAFs increased radiotherapy immunity in lung cancer. Exosomal miR-196a-5p derived from CAFs enhanced radioresistance in lung cancer cells by downregulating NFKBIA, providing a new potential target for the treatment of lung cancer.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 6","pages":"554-564"},"PeriodicalIF":3.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9959751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

miR-29a-3p promotes the regulatory role of eicosapentaenoic acid in the NLRP3 inflammasome and autophagy in microglial cells. miR-29a-3p促进二十碳五烯酸在NLRP3炎性体和小胶质细胞自噬中的调节作用。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-06-01 DOI: 10.1002/kjm2.12670

Jian-Ping Pan, Jia-Li Xie, Li-Yun Huang, Qi-Zhen Wu, Dan-Feng Tang, Qi Jin, Wei Wang, Ming-Fu Yang

{"title":"miR-29a-3p promotes the regulatory role of eicosapentaenoic acid in the NLRP3 inflammasome and autophagy in microglial cells.","authors":"Jian-Ping Pan, Jia-Li Xie, Li-Yun Huang, Qi-Zhen Wu, Dan-Feng Tang, Qi Jin, Wei Wang, Ming-Fu Yang","doi":"10.1002/kjm2.12670","DOIUrl":"https://doi.org/10.1002/kjm2.12670","url":null,"abstract":"Eicosapentaenoic acid (EPA) has been reported to play an anti-inflammatory and antioxidative stress role in a series of human diseases, including major depressive disorder. However, its exact mechanism is still largely unknown. Mouse BV-2 cells were treated with lipopolysaccharide (LPS) to induce an in vitro inflammatory cell model of depression. Cytotoxic effects were assessed with MTT and lactate dehydrigebase release assays. Cytokine mediators were elevated by western blot and enzyme-linked immunosorbent assays. Autophagy-relators were determined by immunofluorescence and western blot analyses. Interaction relationships among molecules were evaluated utilizing chromatin immunoprecipitation and dual luciferase assays. Methylated miR-29a-3p was detected via methylation-specific polymerase chain reaction. EPA treatment at 60 μM had no cytotoxic effects on BV2 cells and significantly inhibited the LPS-induced inflammatory response and NLRP3 inflammasome but activated autophagy, while all these effects were reversed by the autophagy inhibitor 3-MA. Importantly, miR-29a-3p exhibited a role similar to that of EPA in LPS-treated BV2 cells. Mechanistically, EPA treatment elevated miR-29a-3p by repressing its promoter methylation. MAPK8 was a direct target of miR-29a-3p. Inhibition of miR-29a-3p greatly diminished the regulatory roles mediated by EPA in LPS-treated BV2 cells, while these roles were further impeded after MAPK8 silencing. To conclude, our data demonstrated that EPA treatment alleviated LPS-induced NLRP3 inflammasomes by activating autophagy via regulation of miR-29a-3p/MAPK8 signaling, which further elucidates the potential antidepressant mechanism of EPA.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 6","pages":"565-575"},"PeriodicalIF":3.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9658587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The lncRNA HOTAIR attenuates pyroptosis of diabetic cardiomyocytes by recruiting FUS to regulate SIRT3 expression. lncRNA HOTAIR通过募集FUS调节SIRT3表达来减轻糖尿病心肌细胞的焦亡。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-05-01 DOI: 10.1002/kjm2.12676

Jing Xiong, Qing Zhou

{"title":"The lncRNA HOTAIR attenuates pyroptosis of diabetic cardiomyocytes by recruiting FUS to regulate SIRT3 expression.","authors":"Jing Xiong, Qing Zhou","doi":"10.1002/kjm2.12676","DOIUrl":"https://doi.org/10.1002/kjm2.12676","url":null,"abstract":"Diabetic cardiomyopathy (DCM) is a serious cardiovascular complication of diabetes that severely affects the quality of life of diabetic patients. Long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of DCM. However, the role of the lncRNA homeobox transcript antisense RNA (HOTAIR) in the progression of DCM remains unclear. The present study aimed to investigate the role of HOTAIR in high glucose (HG)-induced pyroptosis in cardiomyocytes. The expression of the lncRNA HOTAIR, FUS, and SIRT3 in H9C2 cardiomyocytes was detected by RT-qPCR. Western blotting was used to evaluate the expression of FUS and SIRT3 as well as that of pyroptosis- and inflammation-related proteins. RT-qPCR and ELISA were used to determine the expression and secretion of IL-1β and IL-18. RNA pulldown and RIP experiments were used to validate the binding relationship among HOTAIR, FUS, and SIRT3. Flow cytometry was performed to detect pyroptosis. HG induced pyroptosis and elevated the expression of proteins associated with pyroptosis and inflammation (NLRP3, GSDMD-N, cleaved caspase-1, IL-1β, and IL-18) in cardiomyocytes. HOTAIR and SIRT3 levels were decreased in HG-exposed H9C2 cells. Additionally, overexpression of HOTAIR inhibited the HG-induced pyroptosis and inflammatory response in cardiomyocytes. HOTAIR upregulated SIRT3 expression in H9C2 cells by targeting FUS. Moreover, SIRT3 upregulation suppressed HG-mediated pyroptosis of cardiomyocytes. Notably, SIRT3 depletion reversed the inhibitory effect of HOTAIR on HG-triggered pyroptosis in cardiomyocytes. Our research indicates that HOTAIR alleviates pyroptosis in diabetic cardiomyocytes through the FUS/SIRT3 axis, providing a potential marker for the diagnosis and treatment of DCM.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 5","pages":"458-467"},"PeriodicalIF":3.3,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10066097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Circular RNA circDLG1 (has_circ_0068706) functions as an oncogene in nonsmall cell lung cancer through regulating AKT/mTOR signaling and direct binding to miR-144. 环状RNA circDLG1 (has_circ_0068706)在非小细胞肺癌中作为致癌基因通过调节AKT/mTOR信号传导并直接结合miR-144发挥作用。

IF 3.3 4区医学

Kaohsiung Journal of Medical Sciences Pub Date : 2023-05-01 DOI: 10.1002/kjm2.12662

Yong-Feng Chen, Ai-Ping Xu

{"title":"Circular RNA circDLG1 (has_circ_0068706) functions as an oncogene in nonsmall cell lung cancer through regulating AKT/mTOR signaling and direct binding to miR-144.","authors":"Yong-Feng Chen, Ai-Ping Xu","doi":"10.1002/kjm2.12662","DOIUrl":"https://doi.org/10.1002/kjm2.12662","url":null,"abstract":"Nonsmall cell lung cancer (NSCLC) is a major subtype of lung cancer, causing substantial cancer-related deaths worldwide. However, the molecular basis of NSCLC development and progression remains understudied. Recently, a circular RNA, circDLG1, has been implicated in carcinogenesis and cancer metastasis. Yet, how circDLG1 affects NSCLC progression has not been reported. Here this study aims to elucidate the role of circDLG1 in NSCLC. First, we found that circDLG1 was significantly upregulated in both the GEO dataset and NSCLC tissues. Next, we silenced the expression of circDLG1 in NSCLC cell lines. Knockdown of circDLG1 upregulated miR-144 and downregulated Protein kinase B (AKT)/mechanistic target of rapamycin (mTOR), resulting in suppression of the proliferation activity and metastasis ability of NSCLC. In addition, circDLG1 knockdown significantly decreased the expression of the mesenchymal markers, proliferating cell nuclear antigen (PCNA), and N-cadherin, while increasing the expression level of E-cadherin. In conclusion, we demonstrate that circDLG1 promotes the pathogenesis and progression of NSCLC by regulating the miR-144/AKT/mTOR signaling axis, providing potential diagnostic and therapeutic targets for designing innovative treatment strategies.","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 5","pages":"446-457"},"PeriodicalIF":3.3,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9788980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0