Premium
STAT3 down‐regulation induces mitochondria‐dependent G2/M cell cycle arrest and apoptosis in oesophageal carcinoma cells
Author(s) -
Shao Dan,
Ma Jie,
Zhou Chao,
Zhao JiaNan,
Li LuLu,
Zhao TongJian,
Ai XiLei,
Jiao Ping
Publication year - 2017
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12708
Subject(s) - apoptosis , microbiology and biotechnology , cell cycle , cell growth , cancer research , cell cycle checkpoint , mitochondrion , biology , dna fragmentation , cell , cancer cell , programmed cell death , cancer , biochemistry , genetics
Summary STAT 3 is persistently activated in a wide variety of human tumours, and aberrant STAT 3 activity promotes tumour growth, invasion and metastasis. To explore STAT 3 down‐regulation in human oesophageal cancer cells, cell proliferation, apoptosis and mitochondrial mechanisms were explored in oesophageal carcinoma TE 1 cell cultures. We demonstrate for the first time that STAT 3 down‐regulation by RNA i is sufficient to inhibit oesophageal cancer cell proliferation inducing cell apoptosis. Further, we demonstrate that mitochondrial transmembrane potential is impaired thereby leading to collapsed mitochondrial membrane potential, abnormal mitochondrial membrane depolarization, nuclear DNA fragmentation and cell cycle G2/M arrest under the conditions of STAT 3 down‐regulation. Thus, our results suggest that STAT 3 inhibition is a valid approach to induce oesophageal carcinoma cell mitochondrial‐dependent apoptosis in therapeutic strategies against oesophageal cancers.