scholarly journals ARHGAP6 Promotes Apoptosis and Inhibits Glycolysis in Lung Adenocarcinoma Through STAT3 Signaling Pathway

2020 ◽  
Vol Volume 12 ◽  
pp. 9665-9678
Author(s):  
Pengfei Li ◽  
Huina Lv ◽  
Min Xu ◽  
Bin Zang ◽  
Yegang Ma
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Effect and Mechanism of Interferon-Gamma Combined with Pembrolizumab on Chemoresistance of Lung Adenocarcinoma

2020 ◽  
Vol 10 (1) ◽  
pp. 105-109
Author(s):  
Chunling Peng ◽  
Chunqian Feng ◽  
Sha Feng ◽  
Daiqiang Li
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Western Blot ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Drug Resistant ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Resistant Cells

Tumor microenvironment can lead to chemotherapy resistance in lung cancer. PD-1 and PD-L1 are core regulatory molecules of immune checkpoint. Our study intends to assess IFN-γ combined with Pembrolizumab’s effect on chemoresistance of lung adenocarcinoma. Human A549/DDP lung adenocarcinoma resistant strains were cultured in vitro and randomly divided into control group, IFN-γ group and Pembrolizumab+IFN-γ group followed by analysis of cell proliferation by MTT assay, cell apoptosis by flow cytometry, the levels of PD-L1 and Bcl-2 by Western Blot, the level of interleukin-10 (IL-10) and IL-17 by ELISA, as well as the expression of JAK/STAT3 signaling pathway by Western Blot. IFN-γ-treated A549/DDP cells showed significantly inhibited cell apoptosis, promoted cell proliferation, increased level of IL-10, IL-17, and elevated expression of PD-L1 and Bcl-2, as well as increased phosphorylation of JAK and STAT3 (P < 0.05). However, Pembrolizumab combined with IFN-γ treatment significantly inhibited cell proliferation, increased cell apoptosis, decreased IL-10 and IL-17 level, PD-L1 and Bcl-2 expression as well as JAK and STAT3 phosphorylation with significant difference compared to IFN-γ treatment alone (P < 0.05). IFN-γ up-regulates PD-L1 expression by up-regulating the JAK/STAT3 pathway, inhibits the apoptosis of drug-resistant cells in lung adenocarcinoma, and promotes cell proliferation. Pembrolizumab can reverse IFN-γ’s effect on drug-resistant cells of lung adenocarcinoma, down-regulate JAK/STAT3 signaling pathway and, promote the apoptosis of drug-resistant lung cancer cells, and inhibit cell proliferation.

scholarly journals STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway

2019 ◽  
Vol Volume 11 ◽  
pp. 10061-10072 ◽  
Author(s):  
Xiangjun Guo ◽  
Zhongyi Yan ◽  
Gongming Zhang ◽  
Xiang Wang ◽  
Yun Pan ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Upregulation of miR-216a-5p by Lentinan Targeted Inhibition of JAK2/STAT3 Signaling Pathway to Reduce Lung Adenocarcinoma Cell Stemness, Promote Apoptosis, and Slow Down the Lung Adenocarcinoma Mechanisms

2021 ◽  
Vol 11 ◽  
Author(s):  
Quan Chen ◽  
Yiming Zheng ◽  
Xia Chen ◽  
Pengfei Ge ◽  
Pengcheng Wang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Control Group ◽  
Inhibitory Effects ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Cell Proliferation Activity ◽  
Targeted Inhibition

To investigate the effect of Lentinan (LNT) on lung adenocarcinoma (LUAD) cell stemness and its mechanism. In this study, we founded that LNT significantly reduce the cell proliferation, activity, migration, invasion, and stemness of LUAD cells, and promote their apoptosis compared with the control group in vitro. Moreover, LNT significantly inhibited the volume and weight of tumors of nude mice in vivo. At the same time, LNT can significantly up-regulate miR-216a-5p levels and reduce the protein expression of phospho-JAK2 (Y1007/1008) and phospho-STAT3 (Tyr705), thereby inhibiting the JAK2/STAT3 signaling pathway. Interfering with miR-216a-5p expression and activating the JAK2/STAT3 signaling pathway can significantly reverse LNT inhibitory effects on LUAD. Collectively, LNT can inhibit the JAK2/STAT3 signaling pathway by up-regulating miR-216a-5p, reducing stemness, and promoting LUAD cells apoptosis, then slow down LUAD occurrence and development, providing concepts and experimental foundation treating patients with LUAD.

scholarly journals STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Shu-fen Huo ◽  
Wen-li Shang ◽  
Min Yu ◽  
Xiao-ping Ren ◽  
Hong-xia Wen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Janus Kinase ◽  
Normal Lung ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Abstract Six-transmembrane epithelial antigen of prostate-1 (STEAP1) is a relatively newly identified gene target from prostate cancer, breast cancer, and gastric cancer. However, functions of STEAP1 in lung adenocarcinoma (LUAD) are still unknown. In the present study, we explored the molecular and cellular mechanisms of STEAP1 in LUAD. Western blot and Q-PCR were conducted to detect the protein and mRNA expressions respectively. The cell proliferation was tested by CCK8 assay. The effects of STEAP1 on the metastasis and epithelial–mesenchymal transition (EMT) of LUAD were evaluated by EdU assay, wound healing assay, and transwell migratory assay. H1650, H358, HCC827, H1299, H23, A549, H1693 were selected as human LUAD cell lines in the study. Results have shown that STEAP1 expression was up-regulated in LUAD cells compared with normal lung epithelial cells. Knockdowning of STEAP1 suppressed the proliferation, migration, and invasion of LUAD epithelial cells. Importantly, after comparing the proliferation, migration, and invasion of LUAD to the corresponding control groups treated in STAT3 inhibitor ADZ1480, we found that STEAP1 regulates EMT via Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, STEAP1 can serve as a therapeutic target, and it may have important clinical implications for LUAD treatment.

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