NDLI: Overexpression of microRNA-21 regulating PDCD4 during tumorigenesis of liver fluke-associated cholangiocarcinoma contributes to tumor growth and metastasis

Content Provider	Springer Nature Link
Author	Chusorn, P. Namwat, N. Loilome, W. Techasen, A. Pairojkul, C. Khuntikeo, N. Dechakhamphu, A. Talabnin, C. Chan On, W. Ong, C. K. Teh, B. T. Yongvanit, P.
Copyright Year	2013
Abstract	MicroRNA, an endogenous noncoding RNA modulating gene expression, is a key molecule that by its dysregulation plays roles in inflammatory-driven carcinogenesis. This study aimed to investigate the role of oncomiR miR-21 and its target, the programmed cell death 4 (PDCD4) in tumor growth and metastasis of the liver fluke Opisthorchis viverrini-associated cholangiocarcinoma (CCA). The expression levels of miR-21 and PDCD4 were analyzed using the TaqMan miRNA expression assay and immunohistochemistry in liver tissues of both O. viverrini plus N-nitrosodimethylamine (NDMA)-treated hamsters and human CCA samples (n = 23 cases). The functional assay for miR-21 was performed in CCA cell lines by the anti-miR-21 and pre-miR-21 transfection procedures. The peak of miR-21 levels were reached at 2 (hyperplastic lesions) and 6 (CCA) months of the O. viverrini plus NDMA-induced group and had a reverse response with its target PDCD4 proteins. In human CCA, miR-21 was overexpressed in tumor tissues when compared with nontumor tissues (P = 0.0034) and had a negative correlation with PDCD4 protein (P = 0.026). It was also found that high expression of miR-21 was significantly correlated with shorter survival (P < 0.05) and lymph node metastasis (P = 0.037) of CCA patients. Transient transfection of pre-miR-21 reduced the PDCD4 level and resulted in an increase of M213 CCA cell growth and wound-induced migration ability. These results indicated that miR-21 plays a role in the carcinogenesis and metastasis of O. viverrini-associated CCA by suppressing the function of PDCD4. Modulation of aberrantly expressed miR-21 may be a useful strategy to inhibit tumor cell phenotypes or improve response to chemotherapy.
Starting Page	1579
Ending Page	1588
Page Count	10
File Format	PDF
ISSN	10104283
Journal	Tumor Biology
Volume Number	34
Issue Number	3
e-ISSN	14230380
Language	English
Publisher	Springer Netherlands
Publisher Date	2013-02-17
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Cholangiocarcinoma miR-21 PDCD4 Cell proliferation Metastasis Cancer Research
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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