scholarly journals shRNA-mediated silencing of TARBP2 inhibits NCI-H1299 non-small cell lung cancer cell invasion and migration via the JNK/STAT3/AKT pathway

2016 ◽  
Vol 14 (4) ◽  
pp. 3725-3730 ◽  
Author(s):  
Yue Shi ◽  
Duo Zuo ◽  
Xia Wang ◽  
Meng Han ◽  
Yan Wu
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Invasion ◽  
Small Cell ◽  
Akt Pathway ◽  
Cancer Cell Invasion ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
And Migration

scholarly journals LncRNA MCM3AP-AS1 sponges miR-148a to enhance cell invasion and migration in small cell lung cancer

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hua Luo ◽  
Yukun Zhang ◽  
Guangmei Qin ◽  
Bing Jiang ◽  
Lili Miao
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Invasion ◽  
Small Cell ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
Protein Levels ◽  
Underlying Mechanisms ◽  
And Migration

Abstract Background MCM3AP-AS1 is a recently characterized lncRNA playing an oncogenic role in several cancers. However, its role in lung cancer remains unknown. Here, we aimed to explore the functions of MCM3AP-AS1 in small cell lung cancer (SCLC) and the possible underlying mechanisms. Methods MCM3AP-AS1 and ROCK1 levels in SCLC patients were analyzed by qPCR. RNA pull-down and luciferase assays were performed to analyze the interaction between MCM3AP-AS1 and miR-148a. ROCK1 mRNA and protein levels were detected by qPCR and Western blot, respectively. Cell invasion and migration were analyzed by Transwell assays. Results MCM3AP-AS1 was upregulated in patients with SCLC, and a high MCM3AP-AS1 level was accompanied by a low survival rate. The binding of MCM3AP-AS1 to miR-148a predicted by bioinformatics analysis was verified by RNA pull-down and luciferase assays. However, MCM3AP-AS1 and miR-148a did not affect each other’s expression. ROCK1 was upregulated in SCLC tissues and positively correlated with MCM3AP-AS1. In SCLC cells, MCM3AP-AS1 overexpression increased ROCK1 and promoted cancer cell invasion and migration, while miR-148a overexpression showed the opposite effects and attenuated the effects of MCM3AP-AS1 overexpression on ROCK1 expression and cell behaviors. Conclusions MCM3AP-AS1 sponges miR-148a, thereby increasing SCLC cell invasion and migration via upregulating ROCK1 expression.

RETRACTED: The miR-599 promotes non-small cell lung cancer cell invasion via SATB2

2017 ◽  
Vol 485 (1) ◽  
pp. 35-40 ◽  
Author(s):  
Wenjun Tian ◽  
Guanghai Wang ◽  
Yiqing Liu ◽  
Zhenglan Huang ◽  
Caiqing Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cell ◽  
Cell Lung Cancer ◽  
Cell Invasion ◽  
Small Cell ◽  
Cancer Cell Invasion ◽  
Lung Cancer Cell ◽  
Small Cell Lung

scholarly journals Sphingosine kinase 1 enhances the invasion and migration of non-small cell lung cancer cells via the AKT pathway

2014 ◽  
Vol 33 (3) ◽  
pp. 1257-1263 ◽  
Author(s):  
LIANGMING ZHU ◽  
ZHOU WANG ◽  
YUXIA LIN ◽  
ZHITAO CHEN ◽  
HAIBO LIU ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Sphingosine Kinase ◽  
Small Cell ◽  
Akt Pathway ◽  
Sphingosine Kinase 1 ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Autophagic secretion of HMGB1 from cancer-associated fibroblasts promotes metastatic potential of non-small cell lung cancer cells via NFκB signaling

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Yinghui Ren ◽  
Limin Cao ◽  
Limin Wang ◽  
Sijia Zheng ◽  
Qicheng Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Tumor Cells ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Small Cell ◽  
Cancer Associated Fibroblasts ◽  
Cancer Cell Invasion ◽  
Lung Cancer Cell ◽  
Small Cell Lung

AbstractTumor progression requires the communication between tumor cells and tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs) are major components of stromal cells. CAFs contribute to metastasis process through direct or indirect interaction with tumor cells; however, the underlying mechanism is largely unknown. Here, we reported that autophagy was upregulated in lung cancer-associated CAFs compared to normal fibroblasts (NFs), and autophagy was responsible for the promoting effect of CAFs on non-small cell lung cancer (NSCLC) cell migration and invasion. Inhibition of CAFs autophagy attenuated their regulation on epithelial–mesenchymal transition (EMT) and metastasis-related genes of NSCLC cells. High mobility group box 1 (HMGB1) secreted by CAFs mediated CAFs’ effect on lung cancer cell invasion, demonstrated by using recombinant HMGB1, HMGB1 neutralizing antibody, and HMGB1 inhibitor glycyrrhizin (GA). Importantly, the autophagy blockade of CAFs revealed that HMGB1 release was dependent on autophagy. We also found HMGB1 was responsible, at least in part, for autophagy activation of CAFs, suggesting CAFs remain active through an autocrine HMGB1 loop. Further study demonstrated that HMGB1 facilitated lung cancer cell invasion by activating the NFκB pathway. In a mouse xenograft model, the autophagy specific inhibitor chloroquine abolished the stimulating effect of CAFs on tumor growth. These results elucidated an oncogenic function for secretory autophagy in lung cancer-associated CAFs that promotes metastasis potential, and suggested HMGB1 as a novel therapeutic target.

scholarly journals LncRNA PSMG3-AS1 Downregulates miR-340 through Methylation to Upregulate ROCK1 and Promote Cell Invasion and Migration in Non-small Cell Lung Cancer

2021 ◽  
Author(s):  
Xiyong Wang ◽  
Yang Yang ◽  
Yu Dai ◽  
Hongming Zhang ◽  
Honglin Xia ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Invasion ◽  
Mirna Gene ◽  
Small Cell ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
And Migration

Abstract Background: LncRNA PSMG3‑AS1 plays oncogenic role in breast cancer. However, its role in non-small cell lung cancer (NSCLC) is hardly known. We then studied the role of PSMG3‑AS1 in NSCLC.Methods: RT-qPCR was performed to determine the expression of PSMG3‑AS1 in NSCLC and non-tumor tissues from 60 NSCLC patients. A survival analysis was carried out to visit patients for 5 years to study the role PSMG3‑AS1 in prediction the survival of NSCLC. NSCLC cells were overexpressed with miR-340 or PSMG3‑AS1 to analyze the crosstalk between PSMG3‑AS1 and miR-340. MSP was performed to analyze the methylation of miR-340 miRNA gene. The invasion and migration abilities of cells were determind by Transwell assays.Results: PSMG3‑AS1 was highly expressed in NSCLC and was closely correlated poor survival. PSMG3‑AS1 and miR340 were inversely correlated. In NSCLC cells, PSMG3‑AS1 decreased the expression of miR-340 and increased methylation of miR-340 gene. However, miR-340 overexpression did not significantly affect the expression of PSMG3‑AS1. In addition, PSMG3‑AS1 overexpression resulted in upregulated expression of ROCK1. PSMG3‑AS1 and ROCK1 overexpression increased cell invasion and migration rates. MiR-340 overexpression suppressed cell behaviors and inhibited the role of PSMG3‑AS1.Conclusions: PSMG3‑AS1 may downregulate miR-340 through methylation to upregulate ROCK1 and promote cell invasion and migration in NSCLC.

CCR1 knockdown suppresses human non-small cell lung cancer cell invasion

2008 ◽  
Vol 135 (5) ◽  
pp. 695-701 ◽  
Author(s):  
Chang-Li Wang ◽  
Bing-Sheng Sun ◽  
Yong Tang ◽  
Hong-Qing Zhuang ◽  
Wei-Zhi Cao
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cell ◽  
Cell Lung Cancer ◽  
Cell Invasion ◽  
Small Cell ◽  
Cancer Cell Invasion ◽  
Lung Cancer Cell ◽  
Small Cell Lung
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