microRNA-503 inhibits gastric cancer cell growth and epithelial-to-mesenchymal transition

Abstract

Epithelial-to-mesenchymal transition (EMT) is believed to be associated with cancer cell malignancy, and also to cause cancer invasion and metastasis. Recent evidence indicates that small non-protein coding RNA [microRNAs (miRNAs/miRs)] may act as powerful regulators of EMT. The present study aimed to systematically delineate miR-503 expression in gastric cancer and analyse the function of miR-503 in gastric cancer EMT. In the present study, miR-503 expression was detected in gastric cancer cell lines and gastric cancer tissues by quantitative polymerase chain reaction. Gastric cancer cell migration, invasion and proliferation capabilities were analysed by Transwell, MTT and clonability assays. The expression of mesenchymal markers, including fibronectin, vimentin, N-cadherin, SNAIL and the epithelial marker, E-cadherin, was examined by immunoblot analysis following miR-503 transfection. miR-503 expression was found to be reduced in gastric cancer cell lines compared with normal gastric mucosa cell lines, and the expression of miR-503 was upregulated in non-metastatic-derived gastric cancer cell lines compared with metastatic-derived lines. miR-503 expression levels were significantly reduced in tumour tissues in comparison with adjacent normal mucosa tissues, and the miR-503 expression levels in patients with metastases were significantly lower than those in patients without. miR-503 inhibited gastric cancer cell migration, invasion and proliferation. Fibronectin, vimentin, N-cadherin and SNAIL protein levels were decreased, but E-cadherin expression was increased in an AGS cell line transfected with miR-503. Taken together, the present findings indicate that miR-503 acts as a novel tumour suppressor gene in gastric cancer and can inhibit EMT in gastric cancer cells.

MiR-503 inhibited cell proliferation of human breast cancer cells by suppressing CCND1 expression

“…Aberrant expression of miRNAs has been implicated in a variety of biological processes related to cancer, including proliferation, apoptosis, migration, and invasion, which act as either tumor oncogenes or suppressors [12][13][14][15]. Multiple reports indicated that miR-503 has been showed to be one of the important determinants in cancers [16][17][18][19][20]. However, the relationship between miR-503 and breast cancer remains incompletely understood.…”

miR-503 suppresses metastasis of hepatocellular carcinoma cell by targeting PRMT1

“…It has been reported that miR-503 is downregulated in several tumor types including non-small cell lung cancer [14], oral cancer [15], gastric cancer [16], glioblastoma [17]. In these tumors miR-503 functions as tumor suppressor by repressing oncogene expression.…”

Decreased miR-503 expression in gastric cancer is inversely correlated with serum carcinoembryonic antigen and acts as a potential prognostic and diagnostic biomarker

“…MiR-503 has been identified to downregulate in GC specimens and cell lines 8. In addition, it has been proved as a key modulator of cell biological behaviors in GC: miR-503 inhibits GC cell malignant behaviors and inhibits epithelial–mesenchymal transition (EMT) in GC cells 8.…”

“…In addition, it has been proved as a key modulator of cell biological behaviors in GC: miR-503 inhibits GC cell malignant behaviors and inhibits epithelial–mesenchymal transition (EMT) in GC cells 8. By targeting IGF1R and BCL2, miR-503 sensitizes human GC cell lines to cisplatin of human GC cell lines 9.…”