Chemotherapy is an important treatment for colorectal adenocarcinoma cancer; however, colorectal adenocarcinoma cells often develop resistance to chemotherapeutic drugs, leading to relapse and poor patient prognosis. The development of drug resistance is often a multifactor process, which involved several genes and cellular mechanisms. microRNAs are endogenous small non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. In the present study, we investigated the possible role of microRNAs in regulating drug sensitivity of colorectal adenocarcinoma cells SW620 and SW480. Using microRNA expression arrays and quantitative reverse transcriptase (RT)-PCR, we found that SW620 cells exhibited elevated miR-20a expression compared with SW480 cells. In addition, these two cell lines displayed different sensitivities to the chemotherapeutic drugs fluorouracil, oxaliplatin, and teniposide. Modulation of miR-20a altered the sensitivity of SW620 and SW480 cells to these drugs; knockdown of miR-20a sensitized SW620 cells to chemotherapeutic agents, whereas overexpression of miR-20a in SW480 cells resulted in chemoresistance. Endogenous BNIP2 mRNA and BNIP2 protein levels were inversely related to miR-20a levels as detected by quantitative RT-PCR and western blot analysis. Fluorescence reporter assays showed a direct interaction between miR-20a and the BNIP2 3'UTR. Taken together, our findings suggested that miR-20a may play a role in colorectal adenocarcinoma cancer cell drug resistance and may be a therapeutic target against chemotherapy drug resistance in colorectal adenocarcinoma.

MicroRNAs are an evolutionarily conserved class of endogenous noncoding RNAs that modulate gene expression at the post‐transcriptional level. Recently, microRNA‐23a (miR‐23a) has been found to function as a growth‐promoting and antiapoptotic factor in hepatocellular carcinoma cells. Our previous study showed that miR‐23a was significantly upregulated in gastric adenocarcinoma tissues. In this study, we found that miR‐23a promoted the proliferative potential of gastric adenocarcinoma cell line MGC803. We also identified IL6R as a direct target gene for miR‐23a using a fluorescent reporter assay. The mRNA and protein levels of IL6R were both inversely correlated with the miR‐23a expression level. Our results demonstrate that miR‐23a can target IL6R and promote the growth activity of gastric adenocarcinoma cells in vitro. The downregulation of IL6R by miR‐23a may explain why the suppression of miR‐23a can inhibit gastric cancer cell proliferation.

a b s t r a c tThis study was aimed to investigate miR-216a expression in pancreatic cancer and determine its effects on proliferation. miR-216a was found downregulated in pancreatic cancer tissues as compared to benign pancreatic lesions. JAK2 was identified as a miR-216a gene target. Further, in vivo treatment of PANC-1 tumors with miR-216a reduced JAK2 protein levels in the tumor and reduced tumor volume. In conclusion, miR-216a may function as a tumor suppressor regulating pancreatic cancer cells by targeting the JAK/STAT pathway. Further studies with a larger number of patient samples are necessary to fully explore the diagnostic and therapeutic potential of miR-216a for pancreatic cancer.

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