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Aldo-keto reductase family member C3(AKR1C3)promotes hepatocellular carcinoma cell growth by producing prostaglandin F2α

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Oncology Research 2024年第1期32卷 163-174页

作者： KUO-SHYANG JENG PO-YU CHENG YUEH-HSIEN LIN PO-CHUN LIU PING-HUI TSENG YU-CHAO WANG CHIUNG-FANG CHANG chuen-miin leu Division of General Surgery Far Eastern Memorial HospitalNew Taipei City22060Taiwan Institute of Microbiology and Immunology National Yang Ming Chiao Tung UniversityTaipei City11221Taiwan Institute of Biochemistry and Molecular Biology National Yang Ming Chiao Tung UniversityTaipei City11221Taiwan Institute of Biomedical Informatics National Yang Ming Chiao Tung UniversityTaipei City11221Taiwan Department of Medical Research Far Eastern Memorial HospitalNew Taipei City22060Taiwan

Hepatocellular carcinoma(HCC)is a leading cause of death *** therapies are effective for HCC patients with early disease,but many patients suffer recurrence after surgery and have a poor response to ***,new therapeutic targets are *** analyzed gene expression profiles between HCC tissues and normal adjacent tissues from public databases and found that the expression of genes involved in lipid metabolism was significantly *** analysis showed that AKR1C3 was upregulated in tumors,and high AKR1C3 expression was associated with a poorer prognosis in HCC *** vitro,assays demonstrated that the knockdown of AKR1C3 or the addition of the AKR1C3 inhibitor indomethacin suppressed the growth and colony formation of HCC cell *** of AKR1C3 in Huh7 cells reduced tumor growth in *** explore the mechanism,we performed pathway enrichment analysis,and the results linked the expression of AKR1C3 with prostaglandin F2 alpha(PGF2a)downstream target *** of AKR1C3 activity reduced the production of PGF2a,and supplementation with PGF2a restored the growth of indomethacin-treated Huh7 *** of the PGF receptor(PTGFR)and treatment with a PTGFR inhibitor significantly reduced HCC *** showed that indomethacin potentiated the sensitivity of Huh7 cells to *** summary,our results indicate that AKR1C3 upregulation may promote HCC growth by promoting the production of PGF2α,and suppression of PTGFR limited HCC ***,targeting the AKR1C3-PGF2a-PTGFR axis may be a new strategy for the treatment of HCC.

关键词： Hepatocellular carcinoma Aldo-keto reductase family member C3 Prostaglandin F2 alpha Prostaglandin F receptor

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Nck, a missing adaptor between the B-cell receptor complex and the BCAP/PI3K/Akt pathway

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Cellular & Molecular Immunology 2014年第2期11卷 120-122页

作者： chuen-miin leu Natl Yang Ming Univ Inst Microbiol & Immunol Taipei 11221 Taiwan

The signaling pathways activated by the B-cell antigen receptor （BCR）play a crucial role in the development, activation, and differentiation of B cells. Among them, the activation ofphospha- tidylinositol 3-kinase （PI3K）/Akt is par- ticularly important.1-5 The recruitment of PI3K to the plasma membrane is necessary for the generation ofphospha- tidyl-inositol-3,4,5-triphosphate, which activates PDK1 （Akt/PKB kinase）; in turn, PDK1 activates Akt （Figure 1）.

关键词：肌醇磷酸转移酶类受体抗原细胞膜胰岛素游戏和玩具原癌基因

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Gonadotrophin-releasing hormone-Ⅰ and -Ⅱ stimulate steroidogenesis in prepubertal murine Leydig cells in vitro

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Asian Journal of Andrology 2008年第6期10卷 929-936页

作者： Yung-Ming Lin Ming-Yie Liu Song-Ling Poon Sew-Fen leu Bu-miin Huang Department of Urology College of Medicine National Cheng Kung University Tainan 70101 Taiwan China Department of Environmental and Occupational Health College of Medicine National Cheng Kung University Tainan 70101 Taiwan China Department of Cell Biology and Anatomy College of Medicine National Cheng Kung University Tainan 70101 Taiwan China Institute of Bioindustrial Technology College of Human Ecology HungKuang University Taichung 43302 Taiwan China

Aim： To study the effect and mechanism of gonadotrophin-releasing hormone （GnRH） on murine Leydig cell steroidogenesis. Methods： Purified murine Leydig cells were treated with GnRH-Ⅰ and -Ⅱ agonists, and testosterone production and steroidogenic enzyme expressions were determined. Results： GnRH-Ⅰ and -Ⅱ agonists significantly stimulated murine Leydig cell steroidogenesis 60%-80% in a dose- and time-dependent manner （P 〈 0.05）. The mRNA expressions of steroidogenic acute regulatory （STAR） protein, P450scc, 3β-hydroxysteroid dehydrogenase （HSD）, but not 17β-hydroxylase or 17β-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase （P 〈 0.05）. However, only 3β-HSD protein expression was induced by both GnRH agonists, with a 1.6- to 2-fold increase （P 〈 0.05）. Conclusion： GnRH directly stimulated murine Leydig cell steroidogenesis by activating 3β-HSD enzyme expression.

关键词： gonadotrophin-releasing hormone Leydig cells murine steroidogenesis stimulation

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Apoptotic Effect of Cisplatin and Cordycepin on OC3 Human Oral Cancer Cells

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Chinese Journal of Integrative Medicine 2014年第8期20卷 624-632页

作者： CHEN Ying-hui HAO Lyh-Jyh HUNG Chih-peng CHEN Jung-wei leu Sew-fen HUANG Bu-miin Department of Anesthesia Chi-Mei Medical Center Department of Nursing Min-Hwei College of Health Care Management Division of Endocrinology and Metabolism Kaohsiung Veteran General Hospital Tainan Branch Department of Anesthesiology Chang Gung Memorial Hospital and Kaohsiung Medical CenterChang Gung University Institute of Hot Spring Industry Chia Nan University of Pharmacy and Science Department of Food Science and Technology College of Human EcologyHungKuang University Department of Cell Biology and Anatomy and College of MedicineNational Cheng Kung University

Objective： To evaluate apoptotic effects of cisplatin and cordycepin as single agent or in combination with cytotoxicity in oral cancer cells. Methods： The influences of cisplatin （2.5 μg/mL） and/or cordycapin treatment （10 or 100 μmol/L） to human OC3 oral cancer cell line were investigated by morphological observation for cell death appearance, methylthiazoletetrazolium （MTT） assay for cell viability, flow cytometry assay for cell apoptosis, and Western blotting for apoptotic protein expressions. Results： Data demonstrated that co-administration of cisplatin （2.5 μg/mL） and cordycepin （10 or 100μmol/L） resulted in the enhancement of OC3 cell apoptosis compared to cisplatin or cordycapin alone treatment （24 h）, respectively （P〈0.05）. In flow cytometry assay, percentage of cells arrested at subG1 phase with co-treatment of cordycepin and cisplatin （30%） was significantly higher than cisplatin （5%） or cordycepin （12%） alone group （P〈0.05）, confirming a synergistically apoptotic effect of cordycepin and cisplatin. In cellular mechanism study, co-treatment of cordycepin and cisplatin induced more stress-activated protein kinase/dun terminal kinase （JNK）, the expressions of caspase-7, and the cleavage of poly ADP-ribose polymerase （PARP） as compared to cisplatin or cordycepin alone treatment （P〈0.05）. Conclusion： Cisplatin and cordycepin possess synergistically apoptotic effect through the activation of JNK/caspase-7/PARP pathway in human OC3 oral cancer cell line.

关键词： cisplatin cordycepin apoptosis OC3 synergistic

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