Gemcitabine induces apoptosis via JAK 2 / STAT 3 signaling pathways in lung cancer

Content Provider	Semantic Scholar
Author	Zhang, Ze-Yu Zhang, Yiping Fu, Hai Ying Wang, Jing Zheng, Yong Chao Dong, Qiao Xue
Copyright Year	2016
Abstract	Background: This study was aimed to elucidate the antitumor effect of gemcitabine in lung cancer SPCA-1 cells and the possible molecular mechanism involved. Materials and methods: Cell proliferation was measured by the Cell Count Kit-8 (CCK-8). Cell cycle, apoptosis, reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP) level were assessed by flow cytometry analysis. Real-time PCR and Western blot analysis were used to detect the ratio of Bax/Bcl-2 and the activation of JAK2 and STAT3 after cells were treated with different concentrations of gemcitabine. Results: The results revealed that gemcitabine could inhibit the growth of SPC-A-1 cells significantly in both a time and dose-dependent manner. The cell cycle was blocked and ROS production was increased, while MMP level was decreased after the cells were treated with different concentrations of gemcitabine. Bcl-2 expression was down-regulated remarkably while Bax expression was increased after apoptosis occurred. Additionally, the activation of JAK2 and STAT3 was significantly inhibited in gemcitabine treated SPC-A-1 cells. Conclusions: Gemcitabine may serve as a potential therapeutic agent for lung cancer.
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Language	English
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Content Type	Text
Resource Type	Article