scholarly journals Dietary flavonoid myricetin inhibits invasion and migration of radioresistant lung cancer cells (A549‐IR) by suppressing MMP‐2 and MMP‐9 expressions through inhibition of the FAK‐ERK signaling pathway

2020 ◽  
Vol 8 (4) ◽  
pp. 2059-2067 ◽  
Author(s):  
Hye R. Kang ◽  
Jeong Y. Moon ◽  
Meran K. Ediriweera ◽  
Yeon W. Song ◽  
Moonjae Cho ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Lung Cancer Cells ◽  
Erk Signaling ◽  
Invasion And Migration ◽  
Dietary Flavonoid ◽  
And Migration

Pumilio RNA Binding Family Member 2 Promotes the Proliferation and Metastasis of Lung Cancer Cells by Regulating Ca2+ Signaling Pathway via Targeting C-X-C Chemokine Receptor Type 4

2021 ◽  
Vol 11 (7) ◽  
pp. 1339-1345
Author(s):  
Zhijie Shang ◽  
Yuxuan Wang ◽  
Lixun Chai ◽  
Gengpu Yang
Keyword(s):  
Lung Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Chemokine Receptor ◽  
Rna Binding ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
Proliferation And Metastasis ◽  
And Migration

The aim of the present study was to investigate the mechanism by which pumilio RNA binding family member 2 (PUM2), an RNA-binding protein (RBP) of C-X-C chemokine receptor type 4 (CXCR4), exerts its effects on the development of lung cancer. RT-qPCR and western blot analysis were utilized to measure the expression of PUM2 in several lung cancer cell lines. Cell Counting Kit-8 (CCK-8), colony formation assay, transwell- and wound healing assays were employed to determine the proliferation, invasion and migration of NCI-H520 cells, respectively. Next, the expression of CXCR4 was measured using western blot analysis, and the combination between PUM2 and CXCR4 was verified by RNA immunoprecipitation (RIP) assay and RNA pull down assay. Finally, whether the expression of PUM2 can affect the Ca2+ signaling pathway was confirmed by western blot assay. Results revealed that the expression level of PUM2 was notably upregulated in lung cancer cells, and knockdown of PUM2 significantly inhibited the proliferation, invasion and migration of NCI-H520 cells. PUM2 was confirmed to be the RBP of CXCR4, and PUM2 knockdown decreased the expression of CXCR4. In addition, PUM2 silencing inhibited the phosphorylation of CaMKII, ERK, and MEK. Taken together, these findings demonstrated that PUM2 could promote the proliferation and metastasis of lung cancer cells by regulating Ca2+ signaling pathway via targeting CXCR4, which may provide a novel insight for the future treatment of lung cancer.

Sevoflurane inhibits invasion and migration of lung cancer cells by inactivating the p38 MAPK signaling pathway

2012 ◽  
Vol 26 (3) ◽  
pp. 381-392 ◽  
Author(s):  
Hua Liang ◽  
Miaoning Gu ◽  
Chengxiang Yang ◽  
Hanbing Wang ◽  
Xianjie Wen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals All-Trans Retinoic Acid Induces Proliferation, Survival, and Migration in A549 Lung Cancer Cells by Activating the ERK Signaling Pathway through a Transcription-Independent Mechanism

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Reyna Sara Quintero Barceinas ◽  
Alejandro García-Regalado ◽  
Elena Aréchaga-Ocampo ◽  
Nicolás Villegas-Sepúlveda ◽  
Claudia Haydée González-De la Rosa
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Lung Cancer Cells ◽  
Erk Signaling ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Independent Mechanism ◽  
And Migration

All-trans retinoic acid (ATRA) has been used as an antineoplastic because of its ability to promote proliferation, inhibition, and differentiation, primarily in leukemia; however, in other types of cancer, such as lung cancer, treatment with ATRA is restricted because not all the patients experience the same results. The ERK signaling pathway is dysregulated in cancer cells, including lung cancer, and this dysregulation promotes proliferation and cell invasion. In this study, we demonstrate that treatment with ATRA can activate the ERK signaling pathway by a transcription-independent mechanism through a signaling cascade that involves RARαand PI3K, promoting growth, survival, and migration in lung cancer cells. Until now, this mechanism was unknown in lung cancer cells. The inhibition of the ERK signaling pathway restores the beneficial effects of ATRA, reduces proliferation, increases apoptosis, and blocks the cell migration process in lung cancer cells. In conclusion, our results suggest that the combination of ATRA with ERK inhibitor in clinical trials for lung cancer is warranted.

Prucalopride inhibits lung cancer cell proliferation, invasion, and migration through blocking of the PI3K/AKT/mTor signaling pathway

2019 ◽  
Vol 39 (2) ◽  
pp. 173-181 ◽  
Author(s):  
M Chen ◽  
L-L Zhu ◽  
J-L Su ◽  
G-L Li ◽  
J Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Human Lung ◽  
Mtor Signaling ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Mtor Signaling Pathway ◽  
Invasion And Migration ◽  
And Migration

Lung cancer is the main cause of cancer incidence and mortality around the world. Prucalopride is an agonist for the 5-hydroxytryptamine 4 receptor, but it was unknown whether prucalopride could be used to treat lung cancer. To investigate the biological effects of prucalopride on proliferation, apoptosis, invasion, and migration of lung cancer cells, and its underlying molecular mechanism in the progression of lung cancer, we performed this study. The Cell Counting Kit 8 assay was used to measure the proliferation of A549/A427 lung cancer cells treated with prucalopride. Transwell assay was applied to evaluate cell invasion and migration. Cell apoptosis was detected by flow cytometry and Western blot analyses. The expression levels of related proteins in the PI3K/AKT/mTor signaling pathway were analyzed by Western blotting. Prucalopride inhibited the proliferation, invasion, and migration of A549/A427 human lung cancer cells. It also induced autophagy and apoptosis and decreased the expression of the phosphorylated protein kinase B (AKT) and mammalian target of rapamycin (mTor) in these cells. This study implied an inhibitory role for prucalopride in the progression of human lung cancer.

Knockdown CYP2S1 inhibits lung cancer cells proliferation and migration

2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.

scholarly journals TMEM17 depresses invasion and metastasis in lung cancer cells via ERK signaling pathway

Oncotarget ◽  
2017 ◽  
Vol 8 (41) ◽  
pp. 70685-70694 ◽  
Author(s):  
Xiupeng Zhang ◽  
Yong Zhang ◽  
Yuan Miao ◽  
Haijing Zhou ◽  
Guiyang Jiang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Lung Cancer Cells ◽  
Erk Signaling ◽  
Invasion And Metastasis

scholarly journals Ectopic Production of MDA-7/IL-24 Inhibits Invasion and Migration of Human Lung Cancer Cells

2004 ◽  
Vol 9 (4) ◽  
pp. 510-518 ◽  
Author(s):  
Rajagopal Ramesh ◽  
Isao Ito ◽  
Began Gopalan ◽  
Yuji Saito ◽  
Abner M Mhashilkar ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Invasion And Migration ◽  
Human Lung Cancer Cells ◽  
Ectopic Production ◽  
And Migration

scholarly journals Propolin C Inhibited Migration and Invasion via Suppression of EGFR-Mediated Epithelial-to-Mesenchymal Transition in Human Lung Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-15
Author(s):  
Jih-Tung Pai ◽  
Yi-Chin Lee ◽  
Si-Ying Chen ◽  
Yann-Lii Leu ◽  
Meng-Shih Weng
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Epithelial To Mesenchymal Transition ◽  
Lung Cancer Cells ◽  
Erk Signaling ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion

Controlling lung cancer cell migration and invasion via epithelial-to-mesenchymal transition (EMT) through the regulation of epidermal growth factor receptor (EGFR) signaling pathway has been demonstrated. Searching biological active phytochemicals to repress EGFR-regulated EMT might prevent lung cancer progression. Propolis has been used as folk medicine in many countries and possesses anti-inflammatory, antioxidant, and anticancer activities. In this study, the antimigration and anti-invasion activities of propolin C, a c-prenylflavanone from Taiwanese propolis, were investigated on EGFR-regulated EMT signaling pathway. Cell migration and invasion activities were dose-dependently suppressed by noncytotoxic concentration of propolin C. Downregulations of vimentin and snail as well as upregulation of E-cadherin expressions were through the inhibition of EGFR-mediated phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and extracellular signal-regulated kinase (ERK) signaling pathway in propolin C-treated cells. In addition, EGF-induced migration and invasion were suppressed by propolin C-treated A549 lung cancer cells. No significant differences in E-cadherin expression were observed in EGF-stimulated cells. Interestingly, EGF-induced expressions of vimentin, snail, and slug were suppressed through the inhibition of PI3K/Akt and ERK signaling pathway in propolin C-treated cells. Inhibition of cell migration and invasion by propolin C was through the inhibition of EGF/EGFR-mediated signaling pathway, followed by EMT suppression in lung cancer.

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