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.
Highlights
Colorectal cancer (CRC) is the third most common cancer worldwide [1]
The clinical samples were categorized into less advanced tumor and more advanced tumor. miR-23a was significantly over-expressed in the blood and cancer tissues when compared to the control/normal counterparts
The Western blot analysis showed that the level of apoptosis protease activating factor 1 (APAF1) protein was significantly decreased by 0.51 ± 0.08-fold in SW480 and 0.46 ± 0.17-fold in SW620 following miR-23a mimic transfection and significantly increased by 1.76 ± 0.28-fold in
Summary
Colorectal cancer (CRC) is the third most common cancer worldwide [1]. The carcinogenesis of CRC is heterogeneous, multi-factorial, and may take several decades. MiRNA deregulation in apoptosis contributes to CRC development and resistance to anti-cancer therapy. Over-expression of miR-92a has been reported to cause uncontrollable cell proliferation in CRC via the down-regulation of pro-apoptotic molecule. Programmed cell death 4 (PDCD4), a tumor suppressor protein that is often down-regulated in CRC, is caused by the up-regulation of miR-21 [9,10]. Chang et al has revealed the significance of miR-34a in regulating p53 network of cell cycle control and apoptosis in CRC [11]. Through miRNA microarray study, we had demonstrated that miR-23a may serve as a potential biomarker for the detection of CRC [12]. The focus of this study is to investigate the potentiality of apoptosis resistance function of miR-23a in CRC
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