Affiliations 

  • 1 Department of Surgery, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia. flyong88@yahoo.com
  • 2 Department of Biochemistry, Faculty of Medicine, MAHSA University, Kuala Lumpur 59100, Malaysia. wang.chee@mahsa.edu.my
  • 3 Department of Surgery, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia. aprilroslani@um.edu.my
  • 4 Department of Surgery, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia. drcwlaw@gmail.com
Int J Mol Sci, 2014 Jul 02;15(7):11713-29.
PMID: 24992592 DOI: 10.3390/ijms150711713

Abstract

Recent advances in microRNAome have made microRNAs (miRNAs) a compelling novel class of biomarker in cancer biology. In the present study, the role of miR-23a in the carcinogenesis of colorectal cancer (CRC) was investigated. Cell viability, apoptosis, and caspase 3/7 activation analyses were conducted to determine the potentiality of apoptosis resistance function of miR-23a in CRC. Luciferase assay was performed to verify a putative target site of miR-23a in the 3'-UTR of apoptosis protease activating factor 1 (APAF1) mRNA. The expression levels of miR-23a and APAF1 in CRC cell lines (SW480 and SW620) and clinical samples were assessed using reverse transcription-quantitative real-time PCR (RT-qPCR) and Western blot. We found that the inhibition of miR-23a in SW480 and SW620 cell lines resulted in significant reduction of cell viability and promotion of cell apoptosis. Moreover, miR-23a up-regulation was coupled with APAF1 down-regulation in CRC tissue samples. Taken together, miR-23a was identified to regulate apoptosis in CRC. Our study highlights the potential application of miR-23a/APAF1 regulation axis in miRNA-based therapy and prognostication.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.