Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway release_tltpqkr4knbgpprdqq4pxithu4

by Li-Qiang Qian, Xia-Qin Li, Peng-Hui Ye, Hao-Yuan Su, Gang Wang, Yan Liu, Gen-Hai Shen, Quan-Gen Gao

Published in Oncology Letters by Spandidos Publications.

2017   Volume 14, Issue 4, p4897-4905

Abstract

As an oncogene, MACC1 serves an important function in cancer progression and metastasis. However, the effect of MACC1 in esophageal carcinoma (EC) remains to be fully understood. The present study assessed the association between MACC1 expression and the progression of EC cells. A small interfering (si)RNA was delivered into EC cells to downregulate MACC1 expression. The MTT assay demonstrated that EC cell viability was reduced by siRNA-MACC1. Decreasing MACC1 expression increased the apoptotic rate of EC cells compared with control cells. Transwell and Matrigel assays demonstrated that EC cell migration and invasion, respectively, were downregulated by siRNA-MACC1. Furthermore, knocking down MACC1 suppressed the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway by upregulating the expression of phosphatase and tensin homolog (PTEN), a tumor suppressor. The results of the present study revealed that MACC1 expression affected cellular functions of the EC cells through the PTEN/PI3K/Akt signaling pathway. Therefore, MACC1 may potentially serve as a novel biomarker and therapeutic target for EC.
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Type  article-journal
Stage   published
Date   2017-08-23
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DOI  10.3892/ol.2017.6790
PubMed  29085498
PMC  PMC5649641
Wikidata  Q44451901
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