Interleukin-32 increases human gastric cancer cell invasion associated with tumor progression and metastasis

NCUIR > college of Health Sciences and Technology > Department of Life Science > journal & Dissertation > Item 987654321/102581

Please use this identifier to cite or link to this item: https://ir.lib.ncu.edu.tw/handle/987654321/102581

Title:	Interleukin-32 increases human gastric cancer cell invasion associated with tumor progression and metastasis
Authors:	王陸海;Tsai, Chung-Ying;Wang, Chia-Siu;Tsai, Ming-Ming;Chi, Hsiang-Cheng;Cheng, Wan-Li;Tseng, Yi-Hsin;Chen, Cheng-Yi;Lin, Crystal D.;Wu, Jun-I.;Wang, Lu-Hai;Lin, Kwang-Huei
Contributors:	生醫理工學院生命科學系
Date:	2014-05-01
Issue Date:	2026-04-23 11:13:11 (UTC+8)
Publisher:	American Association for Cancer Research Inc.;American Association for Cancer Research (AACR)
Abstract:	摘要： AbstractPurpose: The proinflammatory cytokine interleukin-32 (IL-32) is a novel tumor marker highly expressed in various human carcinomas, including gastric cancer. However, its effects on prognosis of patients with gastric cancer and cancer metastasis are virtually unknown at present. The main aim of this study was to explore the clinical significance of IL-32 in gastric cancer and further elucidate the molecular mechanisms underlying IL-32–mediated migration and invasion.Experimental Design: Gastric cancer cells with ectopic expression or silencing of IL-32 were examined to identify downstream molecules and establish their effects on cell motility, invasion, and lung metastasis in vivo.Results: IL-32 was significantly upregulated in gastric cancer and positively correlated with aggressiveness of cancer and poor prognosis. Ectopic expression of IL-32 induced elongated morphology and increased cell migration and invasion via induction of IL-8, VEGF, matrix metalloproteinase 2 (MMP2), and MMP9 expression via phosphor-AKT/phospho-glycogen synthase kinase 3β/active β-catenin as well as hypoxia-inducible factor 1α (HIF-1α) signaling pathways. Conversely, depletion of IL-32 in gastric cancer cells reversed these effects and decreased lung colonization in vivo. Examination of gene expression datasets in oncomine and staining of gastric cancer specimens demonstrated the clinical significance of IL-32 and its downstream molecules by providing information on their coexpression patterns.Conclusions: IL-32 contributes to gastric cancer progression by increasing the metastatic potential resulting from AKT, β-catenin, and HIF-1α activation. Our results clearly suggest that IL-32 is an important mediator for gastric cancer metastasis and independent prognostic predictor of gastric cancer. Clin Cancer Res; 20(9); 2276–88. ©2014 AACR. 出版者： American Association for Cancer Research (AACR) 出版日期： 2014-04-30 出處： Clinical Cancer Research, 2014-04, Vol.20 (9), p.2276-2288 識別號： ISSN: 1078-0432 識別號： DOI: 10.1158/1078-0432.ccr-13-1221
Appears in Collections:	[Department of Life Science] journal & Dissertation

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