MicroRNA-20b (miR-20b) Promotes the Proliferation, Migration, Invasion, and Tumorigenicity in Esophageal Cancer Cells via the Regulation of Phosphatase and Tensin Homologue Expression

Abstract

Increasing evidence has indicated that many microRNAs participate in the development and progression of esophageal cancer and gene expression regulation. MicroRNA-20b (miR-20b) has been reported to be aberrantly expressed in various cancers, but its exact role in esophageal cancer cells remains unclear so far. Therefore, we detected the levels of miR-20b in esophageal tumor tissues and their adjacent normal tissues, and various esophageal cancer cell lines by qRT-PCR. We also explored the effects of miR-20b on cell proliferation, migration, invasion and tumorigenicity of esophageal carcinoma cells through transfection with miR-20b mimics or inhibitor to upregulate or downregulate miR-20b expression in the esophageal cancer cells Eca-109 and KYSE-150, respectively. Additionally, the 3'-untranslated region (3'-UTR) of phosphatase and tensin homologue (PTEN) binding with miR-20b was analyzed by dual-luciferase reporter assays. The results indicated that miR-20b expression level in esophageal tumor tissues was significantly increased compared with their neighboring normal tissues, but its expression was inverse with PTEN protein expression. Luciferase assays confirmed that the 3'-UTR of PTEN was a target of miR-20b in esophageal cancer cells. MiR-20b upregulation promoted cell proliferation, migration, invasiveness, and tumor growth, and decreased apoptosis, and reduced PTEN protein level but not mRNA expression in Eca-109 cells. Conversely, downregulation of miR-20b suppressed these processes in KYSE-150 cells, and enhanced PTEN protein expression. These data indicate that miR-20b plays important roles in tumorigenesis of esophageal cancer possibly via regulation of PTEN expression, and it may be a potential therapeutic target for esophageal cancer treatment.

MicroRNA-20b promotes cell proliferation via targeting of TGF-β receptor II and upregulates MYC expression in Ewing's sarcoma cells

“…Although miR-20b may affect gene expression, we regarded TGFBR2 as the target of miR-20b in ES cells. Several studies have detected several target genes of miR-20b, including phosphatase and tensin homolog and matrix metalloproteinase 2 (19,20). Our cDNA array data indicated that TGFBR2 was the only miR-20b-target gene and was uniformly decreased in all five ES cell lines.…”

MiR-543 Promotes Migration, Invasion and Epithelial-Mesenchymal Transition of Esophageal Cancer Cells by Targeting Phospholipase A2 Group IVA

“…Increasing numbers of studies have indicated that miRNAs are involved in various biological processes, such as cell reproduction, differentiation, apoptosis, and metabolism, as well as tumorigenesis [17]. Recently, it has been revealed that altered expression of miRNA contributes to the invasion and metastasis of many cancers [4,6,18].…”

“…Recently, it has been revealed that altered expression of miRNA contributes to the invasion and metastasis of many cancers [4,6,18]. Increasing numbers of studies have indicated that among numerous other miRNAs, miR-543 is also involved in the processes of initiation and maintenance of many kinds of cancers, including ESCC [17]. It has also been reported that miR-543 is down-regulated in breast cancer [19] and endometrial cancer [20] but functions as an oncogene in hepatocellular carcinoma [10,21].…”

“…These different conclusions may be caused by differences in the etiology and pathogenesis of these cancers. Increasing numbers of studies have indicated that a poor survival rate in ESCC patients is highly associated with frequent local invasion and distant metastasis [17]. Furthermore, abnormal …”

“…Cellular Physiology and Biochemistry expression of miRNAs has been implicated in the metastasis and progression of cancers by the acquisition of metastatic potential [17]. However, there have been no reports on the expression of miR-543 in ESCC cells or on the role of miR-543 in the invasion and migration of ESCC cells.…”