The Kaohsiung journal of medical sciences最新文献_第4页

Aptasensor-based point-of-care detection of cardiac troponin biomarkers for diagnosis of acute myocardial infarction. 基于适体传感器的心肌肌钙蛋白生物标志物诊断急性心肌梗死的即时检测。

The Kaohsiung journal of medical sciences Pub Date : 2025-03-01 Epub Date: 2025-01-03 DOI: 10.1002/kjm2.12932

Tharmaraj Vairaperumal, Ping-Yen Liu

引用次数: 0

Telocinobufagin suppresses malignant metastasis of undifferentiated thyroid carcinoma via modulation of the LARP1-mTOR pathway. 端肌球蛋白通过调节LARP1-mTOR通路抑制未分化甲状腺癌的恶性转移。

The Kaohsiung journal of medical sciences Pub Date : 2025-03-01 Epub Date: 2025-01-09 DOI: 10.1002/kjm2.12934

Li-Zhi Qiang, Shi-Zhi Fang

{"title":"Telocinobufagin suppresses malignant metastasis of undifferentiated thyroid carcinoma via modulation of the LARP1-mTOR pathway.","authors":"Li-Zhi Qiang, Shi-Zhi Fang","doi":"10.1002/kjm2.12934","DOIUrl":"10.1002/kjm2.12934","url":null,"abstract":"Metastasis is the trigger of death in anaplastic thyroid cancer (ATC) patients, yet the specific mechanisms at play are still largely enigmatic. While the involvement of LARP1 in the metastatic process of various cancers has been documented, there is a noticeable gap in the literature regarding its potential influence on ATC metastasis. Molecular studies probed LARP1 expression within ATC cells, with subsequent in vitro experiments examining the effects of LARP1 on ATC cell metastasis and the mTOR signaling cascade. A suite of assays, including colony formation, scratch wound healing, transwell invasion, and cell adhesion, was used to assess cell growth, movement, invasion, and attachment. Western Blot determined the expression levels of epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin, N-cadherin) and proteins implicated in metastasis (MMP-2, MMP-9), along with mTOR and p-mTOR. The affinity of Telocinobufagin (TBG) from Yuanhua Toad Essence for LARP1 was investigated through molecular docking, with CETSA assays providing subsequent validation. Further cellular experiments substantiated the influence of TBG on ATC cell metastasis and modulation in the mTOR pathway. LARP1 levels were heightened in ATC cells, and its depletion effectively curbs their proliferative, migratory, invasive, and adhesive activities. With LARP1 knockdown, we also observed that the onset of EMT and metastatic processes was thwarted, as was the mTOR pathway. Subsequent research has uncovered that TBG formed a physical complex with LARP1, allowing it to target and suppress the mTOR pathway, thus preventing the metastasis of ATC. The simultaneous overexpression of LARP1, however, lessened the ability of TBG to inhibit ATC metastasis. This study highlights the importance of TBG binding to LARP1 in the mediation of the mTOR signaling pathway, a key process in the inhibition of ATC cell metastasis. This discovery introduces a new target for the diagnosis of ATC and enlightens the consideration of TBG as a treatment for ATC metastasis.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12934"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960919","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

Dapagliflozin combined with metformin improves blood glucose, bone metabolism and bone mineral density in elderly patients with type 2 diabetes mellitus complicated with osteoporosis. 达格列净联合二甲双胍改善老年2型糖尿病合并骨质疏松患者血糖、骨代谢及骨密度。

The Kaohsiung journal of medical sciences Pub Date : 2025-03-01 Epub Date: 2025-01-15 DOI: 10.1002/kjm2.12937

Haiyan Zheng, Qian Wang, Min Si

{"title":"Dapagliflozin combined with metformin improves blood glucose, bone metabolism and bone mineral density in elderly patients with type 2 diabetes mellitus complicated with osteoporosis.","authors":"Haiyan Zheng, Qian Wang, Min Si","doi":"10.1002/kjm2.12937","DOIUrl":"10.1002/kjm2.12937","url":null,"abstract":"The incidence of type 2 diabetes mellitus (T2DM) complicated with osteoporosis (OP) (T2DM-OP) is growing. Dapagliflozin and metformin are commonly prescribed to manage glycemic levels in T2DM patients. We investigated the clinical efficacy of combining dapagliflozin with metformin in elderly patients with T2DM-OP. Totally 144 T2DM-OP patients were prospectively enrolled and allocated into two groups: the Metformin and Dapagliflozin + Metformin groups. Each group received treatment for 12 months. Fasting peripheral blood samples were collected before and after 12 months of treatment. Glycemic parameters and bone metabolic parameters were measured using oral glucose tolerance test, automatic biochemical analyzers, or liquid chromatography. Bone mineral density (BMD) changes at lumbar vertebrae (L1-4), femoral neck (FN) and total hip (TH) were assessed using dual-energy X-ray bone mineral densitometry. Pain severity was evaluated using the visual analog scale (VAS). The total effective rate, fracture incidence, and adverse reaction rate were also evaluated. After 12 months, both groups showed improvements in glycemic parameters, bone metabolic parameters, and BMD at L1-4, FN, and TH, and reductions in VAS scores. The Dapagliflozin + Metformin group exhibited more significant improvements. The overall effective rate was higher and fracture incidence, was lower in Dapagliflozin + Metformin group, with comparable rates of adverse reactions and safety profiles between the two groups. Taken together, treatment with a combination of dapagliflozin and metformin led to improvements in blood glucose levels, bone metabolism, and BMD in elderly patients with T2DM-OP, demonstrating superior efficacy and safety compared to metformin monotherapy.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12937"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985907","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

hnRNPA2B1 drives colorectal cancer progression via the circCDYL/EIF4A3/PHF8 axis. hnRNPA2B1通过circCDYL/EIF4A3/PHF8轴驱动结直肠癌的进展。

The Kaohsiung journal of medical sciences Pub Date : 2025-03-01 Epub Date: 2025-01-15 DOI: 10.1002/kjm2.12943

Yu-Kai Sun, Jin-Fu Wang, Xi-Wen Sun, Ming Zhang

{"title":"hnRNPA2B1 drives colorectal cancer progression via the circCDYL/EIF4A3/PHF8 axis.","authors":"Yu-Kai Sun, Jin-Fu Wang, Xi-Wen Sun, Ming Zhang","doi":"10.1002/kjm2.12943","DOIUrl":"10.1002/kjm2.12943","url":null,"abstract":"The RNA-binding protein hnRNPA2B1 acts as an m6A reader and plays a role in tumor development. This study investigates the potential mechanism of hnRNPA2B1 in colorectal cancer (CRC) progression. The expression profiles of hnRNPA2B1, circCDYL, and PHF8 in CRC cell lines were analyzed. Following si-hnRNPA2B1 transfection, CRC cell proliferation, invasion, and migration were evaluated by CCK-8 and Transwell. CDYL expression was detected after actinomycin D and RNase R treatment. RIP was conducted to assess the enrichment of hnRNPA2B1 and m6A on circCDYL. RIP and RNA pull-down assays established the interaction between circCDYL and EIF4A3/PHF8. EIF4A3 expression was evaluated using RT-qPCR and Western blot techniques. hnRNPA2B1 and PHF8 displayed high expression levels, whereas circCDYL showed low expression levels in colorectal cancer cells. Inhibition of hnRNPA2B1 reduced CRC cell proliferation, migration, and invasion. hnRNPA2B1 mechanistically elevated the m6A level of circCDYL while decreasing its expression, which in turn reduced the binding of circCDYL to EIF4A3 and enhanced PHF8 expression. In summary, hnRNPA2B1-mediated m6A modification decreases circCDYL expression, which inhibits the interaction of circCDYL with EIF4A3, enhances PHF8 expression, and ultimately facilitates CRC progression.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12943"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985913","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

Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.

The Kaohsiung journal of medical sciences Pub Date : 2025-03-01 Epub Date: 2025-01-07 DOI: 10.1002/kjm2.12933

Bo-Syong Pan, Cheng-Yu Lin, Gilbert Aaron Lee, Hui-Kuan Lin

{"title":"Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.","authors":"Bo-Syong Pan, Cheng-Yu Lin, Gilbert Aaron Lee, Hui-Kuan Lin","doi":"10.1002/kjm2.12933","DOIUrl":"10.1002/kjm2.12933","url":null,"abstract":"SET domain bifurcated histone lysine methyltransferase 1 (SETDB1/ESET), a pivotal H3K9 methyltransferase, has been extensively studied since its discovery over two decades ago. SETDB1 plays critical roles in immune regulation, including B cell maturation, T-cell activity modulation, and endogenous retrovirus (ERV) silencing. While essential for normal immune cell function, SETDB1 overexpression in cancer cells disrupts immune responses by suppressing tumor immunogenicity and facilitating immune evasion. This is achieved through the repression of anti-tumor immune cell production, ERV silencing, and interference with the type I interferon pathway leading to inhibiting immune checkpoint blockade (ICB) efficacy. Beyond its immunological implications, SETDB1 overexpression fosters tumor growth and metastasis via transcriptional silencing of tumor suppressor genes through histone regulation and activating oncogenic signaling by non-histone regulation. These multifaceted roles make SETDB1 an attractive epigenetic target for novel cancer therapies. This review explores SETDB1's dual function in immune regulation and tumor progression, emphasizing its potential in the development of innovative cancer treatments targeting epigenetic dysregulation and oncogenic signaling.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"41 3","pages":"e12933"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598690","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

EZH2-mediated downregulation of miR-155-5p contributes to prostate cancer cell malignancy through SMAD2 and TAB2. ezh2介导的miR-155-5p下调通过SMAD2和TAB2参与前列腺癌细胞恶性。

The Kaohsiung journal of medical sciences Pub Date : 2025-03-01 Epub Date: 2025-01-09 DOI: 10.1002/kjm2.12936

Zhi-Jie Bai, Jia-Yi Liu, Wen-Zhou Xing, Hai-Feng Wang

{"title":"EZH2-mediated downregulation of miR-155-5p contributes to prostate cancer cell malignancy through SMAD2 and TAB2.","authors":"Zhi-Jie Bai, Jia-Yi Liu, Wen-Zhou Xing, Hai-Feng Wang","doi":"10.1002/kjm2.12936","DOIUrl":"10.1002/kjm2.12936","url":null,"abstract":"miR-155 exhibits variable expression in different tumors and fulfills diverse biological roles. However, specific molecular mechanisms by which miR-155-5p, which is under-expressed in prostate cancer (PCa), operates are yet to be elucidated. The role of the enhancer of zeste 2 (EZH2)/miR-155-5p axis in PCa was determined by using bioinformatics tools and performing luciferase reporter assay, chromatin immunoprecipitation PCR, CCK-8 assays, cell migration and invasion assays, RNA isolation, reverse transcription quantity (RT-qPCR) and Western blot. miR-155-5p expression would be reduced and promoter methylation would increase in PCa. After 5-Aza-CdR treatment and the integration of the upstream promoter of miR-155-5p into a pGL3-basic/luciferase construct, fluorescence reporter analysis showed that promoter hypermethylation mediated the suppression of miR-155-5p in PCa. Furthermore, EZH2 attached to the miR-155-5p promoter and modulated its expression. EZH2 facilitated the suppression of miR-155-5p through enhanced H3K27me3 methylation, considerably affecting its expression. Through dual-luciferase assays, SMAD2 and TAB2 were confirmed as downstream targets of miR-155-5p, regulating the PCa cellular phenotype governed by miR-155-5p. Lastly, 5-Aza-CdR regulated miR-155-5p expression by modulating its promoter methylation and influenced the malignant behavior of PCa cells. EZH2 promotes H3K27me3 methylation, repressing miR-155-5p expression, which subsequently upregulates the downstream targets SMAD2 and TAB2 and promotes PCa cell proliferation, epithelial-mesenchymal transition (EMT), migration and invasion.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12936"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960917","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

Successful treatment of a mixed candidal and bacterial skull base osteomyelitis with antimicrobial agents and hyperbaric oxygen therapy-A rare case report. 应用抗菌药物和高压氧治疗成功治疗假丝酵母菌和细菌混合颅底骨髓炎-一例罕见病例报告。

The Kaohsiung journal of medical sciences Pub Date : 2025-03-01 Epub Date: 2025-01-15 DOI: 10.1002/kjm2.12939

Yu-Hsin Liu, Chun-Chieh Wu, Yen-Hsu Chen, Chun-Yu Lin

引用次数: 0

IGF2BP2-induced circRNF20 facilitates breast cancer cell proliferation via the HuR/CDCA4 axis.

The Kaohsiung journal of medical sciences Pub Date : 2025-02-19 DOI: 10.1002/kjm2.12949

Shu-Tao Wu, Xiao-Li Hou, Fei Wang, Wei Sun, Jia-Jie Chen, Ya-Sen Cao, Hong Cheng

{"title":"IGF2BP2-induced circRNF20 facilitates breast cancer cell proliferation via the HuR/CDCA4 axis.","authors":"Shu-Tao Wu, Xiao-Li Hou, Fei Wang, Wei Sun, Jia-Jie Chen, Ya-Sen Cao, Hong Cheng","doi":"10.1002/kjm2.12949","DOIUrl":"https://doi.org/10.1002/kjm2.12949","url":null,"abstract":"This study aimed to explore the mechanism of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) affecting the proliferation of breast cancer (BC) cells. The expression of IGF2BP2, circRNA ring finger protein 20 (circRNF20), and cell division cycle-associated protein 4 (CDCA4) in human BC cells and normal breast epithelial cells was detected via RT-qPCR or Western blotting. After IGF2BP2 expression was altered, CCK-8 assay, colony formation assay, and EdU staining were performed to evaluate changes in the proliferation of BC cells. RNA immunoprecipitation (RIP) assay was used to analyze the binding of circRNF20 to IGF2BP2 or HuR, as well as the binding of HuR to CDCA4. RNA pull-down confirmed the interaction between circRNF20 and HuR. The stability of circRNF20 was tested after treatment with actinomycin D. A nude mouse xenograft tumor model was established to validate the effect of IGF2BP2 in vivo. IGF2BP2, circRNF20, and CDCA4 were highly expressed in BC cells. Silencing IGF2BP2 decreased the proliferation ability of BC cells. Mechanistically, the binding of IGF2BP2 to circRNF20 prevented circRNF20 degradation, thereby promoting the binding of circRNF20 to HuR and increasing the expression of CDCA4. The overexpression of circRNF20 or CDCA4 abolished the inhibitory effect of IGF2BP2 silencing on BC cell proliferation. In conclusion, the binding of IGF2BP2 to circRNF20 prevents its degradation, thus facilitating BC cell proliferation via the HuR/CDCA4 axis.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e12949"},"PeriodicalIF":0.0,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451305","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

A rare case of gastrointestinal diffuse large B cell lymphoma with cold agglutinin disease presentation.

The Kaohsiung journal of medical sciences Pub Date : 2025-02-19 DOI: 10.1002/kjm2.12953

Chin-Mu Hsu, Bi-Hua Du, Ching-Fang Hsu, Hui-Hua Hsiao

引用次数: 0

Correction to "Long non-coding RNA MALAT1 triggers ferroptosis via interaction with FUS to enhance ACSF2 mRNA stabilization in septic acute kidney injury".

The Kaohsiung journal of medical sciences Pub Date : 2025-02-13 DOI: 10.1002/kjm2.12947

引用次数: 0