MiR-16 Induced the Suppression of Cell Apoptosis While Promote Proliferation in Esophageal Squamous Cell Carcinoma

Background/Aims: MicroRNAs (miRNAs) are reported to regulate cell invasion and functions by interfering with the translation of target mRNAs, but the role of miRNAs in esophageal cancer (EC) remains unclear. Methods: RT-PCR and Western blot were used to detect the expression of miRNAs and candidate genes in EC samples (n=89). miR-140 mimics and inhibitor were tansfected in human TE-1 and Eca-109 cells. The transwell assay was used to examine the cell invasive ability. The regulation mechanism was confirmed by luciferase reporter assay. The markers of EMT were detected by using Western blot. Results: miR-140 expression was decreased in the EC tissues compared with the corresponding adjacent tumor tissues. Low expression of miR-140 promotes cell invasion by using transwell assay, while the effect of miR-140 high expression is reverse. Slug, a target gene of miR-140, was examined by luciferase assay and Western blot. Conclusions: miR-140 may regulate the cell invasion of EC via controlling Slug expression.

Section: Discussionmentioning

confidence: 99%

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

Jiang

Zhou

et al. 2014

“…ESCC is the predominant cause of esophageal cancer being responsible for approximately 60-70% of all cases of esophageal cancer worldwide, while EAC accounts for 20-30%, and a number of less common types also occur. However, the incidence of EAC is steadily increasing [7,8]. Any factor which causes chronic irritation and inflammation increases the risk of ESCC, and tobacco and alcohol consumption are therefore well established as the primary risk factors for ESCC [9,10].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Phosphoserine Aminotransferase 1 (PSAT1) Predicts Poor Prognosis and Associates with Tumor Progression in Human Esophageal Squamous Cell Carcinoma

Liu

Jia

Chen

et al. 2016

Background/Aims: Phosphoserine aminotransferase 1 (PSAT1) is over-expressed in many carcinoma tissues, however little is known regarding its expression and function in esophageal carcinogenesis. This study investigated the expression of PSAT1 in human esophageal squamous cell carcinoma (ESCC) tissues to determine the relationship between PSAT1 expression and clinicopathological factors. Methods: The expression of PSAT1 in 64 surgical resections from esophageal carcinogenesis patients was examined by quantitative RT-PCR and immunohistochemistry and the results were compared with clinicopathological factors. In vitro experiments were performed in ESCC cells overexpressing PSAT1 to measure cell viability and invasion. Tumor formation in vivowas examined by injection of tumor cells into immunocompromised mice subcutaneously. Results: PSAT1 expression was elevated in ESCC tissues compared to normal esophageal tissues. Increased PSAT1 expression was significantly associated with stage of disease, lymph node metastasis, distant metastasis and poor prognosis. In vitro, PSAT1 overexpression promoted ESCC cell proliferation and matrigel invasion. In vivo, injection of mice with ECSS cells overexpressing PSAT1 enhanced tumor formation. Western blot analysis revealed that PSAT1 upregulated the expression and/or activity of GSK3β/Snail. Conclusion: PSAT1 plays a crucial role in the development of ESCC and predicts poor survival. Therefore, PSAT1 may be a promising novel anticancer therapeutic target.

“…Recent studies have shown that miRNAs are dysregulated in various cancers, and that their expression is relevant to a diverse array of tumors [42][43][44][45].…”

Section: Discussionmentioning

confidence: 99%

MiR-499 Enhances the Cisplatin Sensitivity of Esophageal Carcinoma Cell Lines by Targeting DNA Polymerase β

Wang

Jiao

Zang

et al. 2015

Background: Human DNA polymerase β (DNA polymerase β, polβ) is a small monomeric protein essential for short-patch base excision repair (BER). It plays an important role in regulating the sensitivity of tumor cells to chemotherapy. Methods: Luciferase reporter and western blot assays were used to determine whether polβ is a major target of miR-499. CCK-8, colony-forming survival and in vivo tumor growth assays were conducted to evaluate if miR-499 can potentially enhance the cisplatin sensitivity and therefore inhibit the proliferation of esophageal cancer (EC) cells. Flow cytometry and immunofluorescence microscopy assays were performed to evaluate whether miR-499 enhance the cisplatin sensitivity and the corresponding apoptosis in EC cells. Results: polβ was pinpointed as a target gene of miR-499. Additionally, we identified that miR-499 can enhance cisplatin's function of inhibiting proliferation and of promoting apoptosis in EC9706 and KYSE30 cell lines. Conclusions: We first investigated whether miR-499 modulates polβ, and observed the influence of miR-499 up-regulation on the sensitivity of EC cell lines to cisplatin treatment. Our study paves the way for more insightful understanding and application of chemotherapy in esophageal cancer in the future.