Abstract
The altered expression of miRNAs is involved in carcinogenesis of esophageal squamous cell carcinoma (ESCC), but whether miRNAs regulate COX-2 expression in ESCC is not clear. To this end, the expression levels of miR-26a and miR-144 in ESCC clinical tissues and cell lines were investigated by qRT-PCR. COX-2 and PEG2 were quantified by western blot and ELISA. Decrease in miR-26a and miR-144 expression in ESCC was found by a comparison between 30 pairs of ESCC tumor and adjacent normal tissues as well as in 11 ESCC cell lines (P < 0.001). Co-transfection of miR-26a and miR-144 in ESCC cell lines more significantly suppressed cell proliferation, migration, and invasion than did either miR-26a or miR-144 alone (all P < 0.001), as shown by assays of CCK8, migration and invasion and flow cytometry. The inhibitory effect of these two miRNAs in vivo was also verified in nude mice xenograft models. COX-2 was confirmed as a target of miR-26a and miR-144. In conclusion, miR-26a and miR-144 expression is downregulated in ESCC. Co-expression of miR-26a and miR-144 in ESCC cells resulted in inhibition of proliferation and metastasis in vitro and in vivo, suggesting that targeting COX-2 may be the mechanism of these two miRNAs.
Highlights
Esophageal carcinoma is the eighth most common cancer worldwide and the sixth leading cause of cancer death [1]
Apoptosis and cell cycle arrest in cells stably transfected with miR-26a, miR-144, or both were analyzed via flow cytometry
We investigated the effect of miR-26a and miR-144 on human esophageal squamous cell carcinoma (ESCC)
Summary
Esophageal carcinoma is the eighth most common cancer worldwide and the sixth leading cause of cancer death [1]. Esophageal squamous cell carcinoma (ESCC) is a common type of esophageal cancer in China—about 210 000 patients die each year of ESCC, or 52% of all ESCC deaths worldwide [2]. It is important to delineate the potential mechanisms of tumor development, to find novel therapeutic targets for ESCC. COX-1 is constitutively expressed in most tissues, while COX-2 is the inducible isoform, which is responsible for the elevated production of prostaglandins in response to various inflammatory stimuli, hormones, and growth factors [4]. Accumulating evidence supports that COX-2 is involved in both tumor development and progression [5,6,7,8,9,10], including ESCC [11,12,13,14,15,16]. Cell proliferation was measured with a Cell Counting Kit-8 (CCK-8, Dojindo, Japan). The absorbance at 450 nm was measured with a plate reader
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