Downregulation of miR-29b targets DNMT3b to suppress cellular apoptosis and enhance proliferation in pancreatic cancer

Autor: Ju Huang, Chun‑Yu Zhao, Cheng Rong Wu, Li‑Hua Wang, Liu Ye Huang, Jun Cui, Zhi‑Zhi Xing
Jazyk: angličtina
Rok vydání: 2017
Předmět:
0301 basic medicine
Male
Cancer Research
Methyltransferase
pancreatic cancer
Gene Expression
Apoptosis
medicine.disease_cause
Biochemistry
DNA Methyltransferase 3A
Mice
0302 clinical medicine
Genes
Reporter
DNA (Cytosine-5-)-Methyltransferases
3' Untranslated Regions
Gene knockdown
Chemistry
Articles
Cell cycle
Immunohistochemistry
microRNA-29b
Gene Expression Regulation
Neoplastic
Oncology
030220 oncology & carcinogenesis
Gene Knockdown Techniques
embryonic structures
Disease Progression
Molecular Medicine
RNA Interference
Cell Survival
DNA methyltransferase 3b
03 medical and health sciences
Pancreatic cancer
Cell Line
Tumor
Genetics
medicine
Animals
Humans
Viability assay
Molecular Biology
Cell Proliferation
Oncogene
Cancer
medicine.disease
Pancreatic Neoplasms
Disease Models
Animal
MicroRNAs
030104 developmental biology
Cancer research
Carcinogenesis
Zdroj: Molecular Medicine Reports
ISSN: 1791-3004
1791-2997
Popis: As one of the most aggressive types of tumor, pancreatic cancer is a principal cause of tumor‑associated mortality. Negative associations between microRNA‑29 (miR‑29) and DNA methyltransferases (DNMT) 3a and 3b have been demonstrated to be associated with the carcinogenesis of a number of types of cancer; however, this has not been completely elucidated in pancreatic cancer. In the present study, pancreatic cancer tissues (n=15) and corresponding paracancerous tissues (n=15) were obtained and the results of reverse transcription‑quantitative polymerase chain reaction analysis indicated decreased expression of miR‑29b and enhanced mRNA expression of DNMT3b in pancreatic cancer tissues, compared with the corresponding paracancerous tissues. Increased protein expression of DNMT3b was demonstrated by western blotting and immunohistochemistry. In addition, the negative association between miR‑29b and DNMT3b was noted in pancreatic cancer tissues, and luciferase reporter assays confirmed that miR‑29b was able to directly target DNMT3b in vitro. Notably, miR‑29b overexpression was able to decrease cell viability and to promote the apoptosis by targeting DNMT3b, and the knockdown of DNMT3b exhibited consistent results in vitro and in vivo. The results of the present study suggested that miR‑29b, as a tumor suppressor, may be a novel target for the development of treatments for pancreatic cancer.
Databáze: OpenAIRE
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