scholarly journals Ang-2 promotes lung cancer metastasis by increasing epithelial-mesenchymal transition

Oncotarget ◽  
2018 ◽  
Vol 9 (16) ◽  
pp. 12705-12717 ◽  
Author(s):  
Zhizhen Dong ◽  
Jianrong Chen ◽  
Xuli Yang ◽  
Wenjie Zheng ◽  
Li Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Lung Cancer Metastasis

Nm23-H1 inhibits hypoxia induced epithelial-mesenchymal transition and stemness in non-small cell lung cancer cells

2019 ◽  
Vol 400 (6) ◽  
pp. 765-776 ◽  
Author(s):  
Cun-en Wu ◽  
Yu-wen Zhuang ◽  
Jin-yong Zhou ◽  
Shen-lin Liu ◽  
Xi Zou ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Small Cell ◽  
Small Cell Lung ◽  
Mesenchymal Transition ◽  
Lung Cancer Metastasis ◽  
Allelic Deletion

Abstract The Nm23 gene has been acknowledged to play a crucial role in lung cancer metastasis inhibitory cascades controlled by multiple factors. Low expression or allelic deletion of nm23-H1 is strongly linked to widespread metastasis and poor differentiation of non-small cell lung cancer (NSCLC). In this study, nm23-H1 was down regulated in epithelial-mesenchymal transition (EMT) and stemness enhancement under cobalt chloride (CoCl2)-induced hypoxia in NSCLC cells. Moreover, knocking down of nm23-H1 by shRNA apparently promoted hypoxia induced EMT and stemness, which was entirely suppressed via over expression of nm23-H1. Mechanistically, the Wnt/β-catenin signaling pathway was found to participate in the nm23-H1-mediated process. Besides, XAV939 prohibited cell EMT and stemness which could be impaired by knocking down of nm23-H1, while stable transfection of nm23-H1 attenuated hypoxia phonotype induced by lithium chloride (LiCl). Generally, our experiment provided evidence that nm23-H1 can reverse hypoxia induced EMT and stemness through the inhibition of the Wnt/β-catenin pathway, which may furnish a deeper perspective into the better treatment or prognosis for NSCLC.

scholarly journals Daxx inhibits hypoxia-induced lung cancer cell metastasis by suppressing the HIF-1α/HDAC1/Slug axis

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Ching-Wen Lin ◽  
Lu-Kai Wang ◽  
Shu-Ping Wang ◽  
Yih-Leong Chang ◽  
Yi-Ying Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cell ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Hypoxia Inducible Factor ◽  
Cancer Invasion ◽  
Death Domain ◽  
Mesenchymal Transition ◽  
Histone Deacetylase 1 ◽  
Lung Cancer Metastasis

Abstract Hypoxia is a major driving force of cancer invasion and metastasis. Here we show that death domain-associated protein (Daxx) acts to negatively regulate hypoxia-induced cell dissemination and invasion by inhibiting the HIF-1α/HDAC1/Slug pathway. Daxx directly binds to the DNA-binding domain of Slug, impeding histone deacetylase 1 (HDAC1) recruitment and antagonizing Slug E-box binding. This, in turn, stimulates E-cadherin and occludin expression and suppresses Slug-mediated epithelial–mesenchymal transition (EMT) and cell invasiveness. Under hypoxic conditions, stabilized hypoxia-inducible factor (HIF)-1α downregulates Daxx expression and promotes cancer invasion, whereas re-expression of Daxx represses hypoxia-induced cancer invasion. Daxx also suppresses Slug-mediated lung cancer metastasis in an orthotopic lung metastasis mouse model. Using clinical tumour samples, we confirmed that the HIF-1α/Daxx/Slug pathway is an outcome predictor. Our results support that Daxx can act as a repressor in controlling HIF-1α/HDAC1/Slug-mediated cancer cell invasion and is a potential therapeutic target for inhibition of cancer metastasis.

scholarly journals MiRNAs and LncRNAs: Dual Roles in TGF-β Signaling-Regulated Metastasis in Lung Cancer

2020 ◽  
Vol 21 (4) ◽  
pp. 1193 ◽  
Author(s):  
Xing-Ning Lai ◽  
Jun Li ◽  
Li-Bo Tang ◽  
Wen-Tong Chen ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Metastasis ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Circular Rnas ◽  
High Morbidity ◽  
Dual Roles ◽  
Mesenchymal Transition ◽  
Lung Cancer Metastasis ◽  
Non Coding Rnas

Lung cancer is one of the most malignant cancers around the world, with high morbidity and mortality. Metastasis is the leading cause of lung cancer deaths and treatment failure. MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs), two groups of small non-coding RNAs (nc-RNAs), are confirmed to be lung cancer oncogenes or suppressors. Transforming growth factor-β (TGF-β) critically regulates lung cancer metastasis. In this review, we summarize the dual roles of miRNAs and lncRNAs in TGF-β signaling-regulated lung cancer epithelial-mesenchymal transition (EMT), invasion, migration, stemness, and metastasis. In addition, lncRNAs, competing endogenous RNAs (ceRNAs), and circular RNAs (circRNAs) can act as miRNA sponges to suppress miRNAs, thereby mediating TGF-β signaling-regulated lung cancer invasion, migration, and metastasis. Through this review, we hope to cast light on the regulatory mechanisms of miRNAs and lncRNAs in TGF-β signaling-regulated lung cancer metastasis and provide new insights for lung cancer treatment.

Melatonin suppresses lung cancer metastasis by inhibition of epithelial–mesenchymal transition through targeting to Twist

2019 ◽  
Vol 133 (5) ◽  
pp. 709-722 ◽  
Author(s):  
Chia-Chia Chao ◽  
Po-Chun Chen ◽  
Pei-Chen Chiou ◽  
Chin-Jung Hsu ◽  
Po-I Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Stage ◽  
Bhlh Transcription Factor ◽  
Mesenchymal Transition ◽  
Lung Cancer Metastasis ◽  
Twist Expression ◽  
Carcinogenic Substances

AbstractThe epithelial–mesenchymal transition (EMT) phenotype, whereby mature epithelial cells undergo phenotype transition and differentiate into motile, invasive cells, has been indicated in tumor metastasis. The melatonin hormone secreted by the pineal gland has an antioxidant effect and protects cells against carcinogenic substances that reduce tumor progression. However, the effects of melatonin in EMT and lung cancer metastasis are largely unknown. We found that melatonin down-regulated EMT by inhibiting Twist/Twist1 (twist family bHLH transcription factor 1) expression. This effect was mediated by MT1 receptor, PLC, p38/ERK and β-catenin signaling cascades. Twist expression was positively correlated with tumor stage and negatively correlated with MT1 expression in lung cancer specimens. Furthermore, melatonin inhibited EMT marker expression and lung cancer metastasis to liver in vivo. Finally, melatonin shows promise in the treatment of lung cancer metastasis and deserves further study.

scholarly journals PGC1α Loss Promotes Lung Cancer Metastasis through Epithelial-Mesenchymal Transition

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1772
Author(s):  
Taek-In Oh ◽  
Mingyu Lee ◽  
Yoon-Mi Lee ◽  
Geon-Hee Kim ◽  
Daekee Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pancreatic Cancer ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Lung Cancer ◽  
Poor Survival ◽  
Mesenchymal Transition ◽  
Lung Cancer Metastasis ◽  
Metastatic Lung

PGC1α oppositely regulates cancer metastasis in melanoma, breast, and pancreatic cancer; however, little is known about its impact on lung cancer metastasis. Transcriptome and in vivo xenograft analysis show that a decreased PGC1α correlates with the epithelial–mesenchymal transition (EMT) and lung cancer metastasis. The deletion of a single Pgc1α allele in mice promotes bone metastasis of KrasG12D-driven lung cancer. Mechanistically, PGC1α predominantly activates ID1 expression, which interferes with TCF4-TWIST1 cooperation during EMT. Bioinformatic and clinical studies have shown that PGC1α and ID1 are downregulated in lung cancer, and correlate with a poor survival rate. Our study indicates that TCF4-TWIST1-mediated EMT, which is regulated by the PGC1α-ID1 transcriptional axis, is a potential diagnostic and therapeutic target for metastatic lung cancer.

NEDD9 promotes lung cancer metastasis through epithelial-mesenchymal transition

2013 ◽  
Vol 134 (10) ◽  
pp. 2294-2304 ◽  
Author(s):  
Yujuan Jin ◽  
Fei Li ◽  
Chao Zheng ◽  
Ye Wang ◽  
Zhaoyuan Fang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Lung Cancer Metastasis
Sign in / Sign up

Export Citation Format

Share Document