scholarly journals FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway

RSC Advances ◽  
2018 ◽  
Vol 8 (59) ◽  
pp. 33786-33793
Author(s):  
Pei Wang ◽  
Hongbing Ma ◽  
Yong Li ◽  
Dong Chen ◽  
Xiaohui Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
A549 Cell ◽  
Cell Apoptosis ◽  
Premature Death

Lung cancer begins in the lung and is a leading cause of premature death.

scholarly journals Retraction: FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4572-4572
Author(s):  
Laura Fisher
Keyword(s):  
Signaling Pathway ◽  
A549 Cell ◽  
Cell Apoptosis

Retraction of ‘FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway’ by Pei Wang et al., RSC Adv., 2018, 8, 33786–33793, DOI: 10.1039/C8RA06041J.

scholarly journals Knockdown of microRNA-126 Suppresses Non-Small-Cell Lung Cancer via Inhibiting PI3K-AKT-mTOR Pathway

2021 ◽  
Author(s):  
Panfeng Chen ◽  
Ping Jiang ◽  
Xi Yu ◽  
Min Yang
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Cancer Tissue ◽  
Potential Therapeutic Target ◽  
Lung Cancer Patients ◽  
Novel Drugs ◽  
Healthy Control ◽  
Pi3k Signaling Pathway ◽  
Nsclc Patients

Abstract Background As one of the most common cause of cancer death in the world, lung cancer causes approximate 1.6 million deaths annually. Among, NSCLC accounts approximately 85% of patients in whole lung cancer patients. As one of miRNAs, miR-126 closely involves in pathogenesis of several types of cancers including colorectal, prostate, bladder and gastric cancer, and so on. Thus, the present study aims to investigate effects of miR126 on pathogenesis of NSCLC. In the study, two lung cancer cell lines including A549 and H1650 were used. Results It was found that expression of miR126 was decreased in PBMC of NSCLC patients compared to healthy control. Expression of miR126 was decreased in cancer tissue compared to paracancerous tissues in NSCLC patients. MiR-126 KD remarkably increased expression of apoptosis genes including caspase3 and capsae9, and decreased cell viability in lung cancer cells including A549 and H1650 cells. Interesting, In Silico analysis indicated that miR-126 could target PI3K signaling pathway, which was confirmed by WB assay. KD of PI3KR2 compromised promotion of miR-126 on cell apoptosis. Similarly, it was found that KD of mTOR compromised promotion of miR-126 on cell apoptosis. Conclusions Thus, the present study confirmed that miR-126 plays an important role in apoptosis of lung cells via mTOR signaling pathway. miR-126 might be a potential therapeutic target for developing novel drugs against NSCLC.

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 Integrated High Throughput Analysis Identifies GSK3 as a Crucial Determinant of p53-Mediated Apoptosis in Lung Cancer Cells

2017 ◽  
Vol 42 (3) ◽  
pp. 1177-1191 ◽  
Author(s):  
Yu Zhang ◽  
Chenyang Zhu ◽  
Bangyao Sun ◽  
Jiawei Lv ◽  
Zhonghua Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
A549 Cell ◽  
Cell Apoptosis ◽  
Integrated Analysis ◽  
Dependent Manner ◽  
Cell Lung Carcinoma ◽  
Synthetic Lethal ◽  
Genome Wide ◽  
Genome Wide Gene Expression

Background/Aims: p53 dysfunction is frequently observed in lung cancer. Although restoring the tumour suppressor function of p53 is recently approved as a putative strategy for combating cancers, the lack of understanding of the molecular mechanism underlying p53-mediated lung cancer suppression has limited the application of p53-based therapies in lung cancer. Methods and Results: Using RNA sequencing, we determined the transcriptional profile of human non-small cell lung carcinoma A549 cells after treatment with two p53-activating chemical compounds, nutlin and RITA, which could induce A549 cell cycle arrest and apoptosis, respectively. Bioinformatics analysis of genome-wide gene expression data showed that distinct transcription profiles were induced by nutlin and RITA and 66 pathways were differentially regulated by these two compounds. However, only two of these pathways, 'Adherens junction' and 'Axon guidance', were found to be synthetic lethal with p53 re-activation, as determined via integrated analysis of genome-wide gene expression profile and short hairpin RNA (shRNA) screening. Further functional protein association analysis of significantly regulated genes associated with these two synthetic lethal pathways indicated that GSK3 played a key role in p53-mediated A549 cell apoptosis, and then gene function study was performed, which revealed that GSK3 inhibition promoted p53-mediated A549 cell apoptosis in a p53 post-translational activity-dependent manner. Conclusion: Our findings provide us with new insights regarding the mechanism by which p53 mediates A549 apoptosis and may cast light on the development of more efficient p53-based strategies for treating lung cancer.

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