scholarly journals Dioscin overcome TKI resistance in EGFR-mutated lung adenocarcinoma cells via down-regulation of tyrosine phosphatase SHP2 expression

2018 ◽  
Vol 14 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Yao-Chen Wang ◽  
De-Wei Wu ◽  
Tzu-Chin Wu ◽  
Lee Wang ◽  
Chih-Yi Chen ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Tyrosine Phosphatase ◽  
Down Regulation ◽  
Adenocarcinoma Cells ◽  
Tki Resistance ◽  
Lung Adenocarcinoma Cells ◽  
Egfr Mutated

scholarly journals Semaphorin 7A promotes EGFR-TKI resistance in EGFR mutant lung adenocarcinoma cells

JCI Insight ◽  
2018 ◽  
Vol 3 (24) ◽  
Author(s):  
Yuhei Kinehara ◽  
Izumi Nagatomo ◽  
Shohei Koyama ◽  
Daisuke Ito ◽  
Satoshi Nojima ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
Tki Resistance ◽  
Lung Adenocarcinoma Cells ◽  
Egfr Mutant ◽  
Egfr Tki

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

2020 ◽  
Author(s):  
Shao-Hui Yan ◽  
Shu-Feng Xu ◽  
Lei Zheng ◽  
Li-Ying Kang ◽  
Jun-Li Cao ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Tyrosine Phosphatase ◽  
Negative Control ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Blank Group ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Abstract Background The study aimed to investigate the effect and mechanism of miR-186, which targets protein tyrosine phosphatase (Shp2) PI3K/Akt/mTOR signaling pathway, on the biological characteristics of lung adenocarcinoma cells. Methods In this experimental study, Human lung adenocarcinoma cell line SPC-A-1 was grouped as Blank group, negative control (NC) group, miR-186 mimic group, miR-186 inhibitor group, si-Shp2 group and miR-186 inhibitor+si-Shp2 group. Results The results showed that miR-186 can target and down-regulate the expression of Shp2 gene. Compared with the Blank group, levels of Shp2, N-cadherin and Bcl-2 and level of PI3K/p-PI3K, Akt/P-Akt, mTOR/p-mTOR as well as cell proliferation, migration and invasion ability and the proportion of cells in S phase significantly decreased in the miR-186 mimic group and the si-Shp2 group, while the levels of E-cadherin and Bax as well as the proportion of cells in G1 phase and cell gene and mediates apoptosis rate increased significantly (all P < 0.05). Compared with the miR-186 inhibitor group, the miR-186 inhibitor + si-Shp2 group showed similar trend in all parameters with the comparison above (all P < 0.05). Conclusions The overexpression of miR-186 can down-regulate Shp2 gene expression, further inhibit the proliferation, invasion and migration and promote apoptosis of lung adenocarcinoma cells by inhibiting the activation of PI3K/Akt/mTOR signaling pathway.

scholarly journals Overexpression of RhoV Promotes the Progression and EGFR-TKI Resistance of Lung Adenocarcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Hongjin Chen ◽  
Ruixue Xia ◽  
Long Jiang ◽  
Yong Zhou ◽  
Haojun Xu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Rho Gtpases ◽  
Rho Gtpase ◽  
Critical Role ◽  
Migration And Invasion ◽  
Tumor Cell Migration ◽  
Adenocarcinoma Cells ◽  
Tki Resistance ◽  
Lung Adenocarcinoma Cells ◽  
Egfr Tki

BackgroundThe Rho GTPase family with ~20 member genes play central roles in a wide variety of cellular processes and tumor cell migration and metastasis. Different Rho GTPase may play different roles in the progression of lung adenocarcinoma.MethodsWe comprehensively examined the expression of all Rho GTPase family member genes in a panel of lung adenocarcinoma patient’s tumors and matched normal tissues. We next investigated the critical role of RhoV in different lung adenocarcinoma cells and animal models.ResultsRhoV was identified as one of the most significantly overexpressed Rho GTPases in lung adenocarcinoma and associated with patients’ survival. Silencing RhoV expression inhibits proliferation, migration and invasion, and tumorigenicity capacities of lung adenocarcinoma cells. Moreover, knockdown RhoV promoted the sensitivity of EGFR-TKI in the gefitinib resistant PC9 cells (PC9-GR) and aggravated gefitinib-induced lung cancer cell apoptosis both in PC9 and PC9-GR cells. Our data also indicated that RhoV induced progression and EGFR-TKI resistance of lung adenocarcinoma may be related to the activation of the AKT/ERK pathway.ConclusionOverexpression of RhoV in lung adenocarcinoma promotes the progression and EGFR-TKI resistance, suggesting RhoV is a promising prognosis and therapeutic target of lung adenocarcinoma.

scholarly journals PFKFB4 promotes lung adenocarcinoma progression via phosphorylating and activating transcriptional coactivator SRC-2

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiguang Meng ◽  
Xuxin Chen ◽  
Zhihai Han
Keyword(s):  
Lung Adenocarcinoma ◽  
Transcriptional Activity ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Transcriptional Coactivator ◽  
Downstream Target ◽  
Steroid Receptor Coactivator ◽  
Adenocarcinoma Cells ◽  
Family Protein ◽  
Lung Adenocarcinoma Cells

Abstract Background To investigate the role and its potential mechanism of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 (PFKFB4) in lung adenocarcinoma. Methods Co-immunoprecipitation was performed to analyze the interaction between PFKFB4 and SRC-2. Western blot was used to investigate the phosphorylation of steroid receptor coactivator-2 (SRC-2) on the condition that PFKFB4 was knockdown. Transcriptome sequencing was performed to find the downstream target of SRC-2. Cell Counting Kit-8 (CCK-8) assay, transwell assay and transwell-matrigel assay were used to examine the proliferation, migration and invasion abilities in A549 and NCI-H1975 cells with different treatment. Results In our study we found that PFKFB4 was overexpressed in lung adenocarcinoma associated with SRC family protein and had an interaction with SRC-2. PFKFB4 could phosphorylate SRC-2 at Ser487, which altered SRC-2 transcriptional activity. Functionally, PFKFB4 promoted lung adenocarcinoma cells proliferation, migration and invasion by phosphorylating SRC-2. Furthermore, we identified that CARM1 was transcriptionally regulated by SRC-2 and involved in PFKFB4-SRC-2 axis on lung adenocarcinoma progression. Conclusions Our research reveal that PFKFB4 promotes lung adenocarcinoma cells proliferation, migration and invasion via enhancing phosphorylated SRC-2-mediated CARM1 expression.

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