scholarly journals TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Suhong Zhang ◽  
Haiting Dai ◽  
Wenya Li ◽  
Runming Wang ◽  
Hanyu Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Motility ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Cancer Metastasis ◽  
Human Cancer ◽  
Transmembrane Protein ◽  
Oncogenic Signaling ◽  
Cancer Cell Motility ◽  
Human Cancer Cells

AbstractTransmembrane protein (TMEM) is a family of protein that spans cytoplasmic membranes and allows cell–cell and cell–environment communication. Dysregulation of TMEMs has been observed in multiple cancers. However, little is known about TMEM116 in cancer development. In this study, we demonstrate that TMEM116 is highly expressed in non-small-cell lung cancer (NSCLC) tissues and cell lines. Inactivation of TMEM116 reduced cell proliferation, migration and invasiveness of human cancer cells and suppressed A549 induced tumor metastasis in mouse lungs. In addition, TMEM116 deficiency inhibited PDK1-AKT-FOXO3A signaling pathway, resulting in accumulation of TAp63, while activation of PDK1 largely reversed the TMEM116 deficiency induced defects in cancer cell motility, migration and invasive. Together, these results demonstrate that TMEM116 is a critical integrator of oncogenic signaling in cancer metastasis.

scholarly journals Lichen Secondary Metabolite, Physciosporin, Inhibits Lung Cancer Cell Motility

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0137889 ◽  
Author(s):  
Yi Yang ◽  
So-Yeon Park ◽  
Thanh Thi Nguyen ◽  
Young Hyun Yu ◽  
Tru Van Nguyen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Motility ◽  
Secondary Metabolite ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cancer Cell Motility

scholarly journals Alpha-Actinin 4 Is Associated with Cancer Cell Motility and Is a Potential Biomarker in Non–Small Cell Lung Cancer

2015 ◽  
Vol 10 (2) ◽  
pp. 286-301 ◽  
Author(s):  
Ming-Chuan Wang ◽  
Ying-Hua Chang ◽  
Chih-Chieh Wu ◽  
Yu-Chang Tyan ◽  
Hua-Chien Chang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cancer Cell Motility ◽  
Potential Biomarker

scholarly journals Knockdown of Rab5a expression decreases cancer cell motility and invasion through integrin-mediated signaling pathway

2011 ◽  
Vol 18 (1) ◽  
pp. 58 ◽  
Author(s):  
Shan-shan Liu ◽  
Xiang-mei Chen ◽  
Hong-xia Zheng ◽  
Shu-liang Shi ◽  
Yu Li
Keyword(s):  
Cell Motility ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Cancer Cell Motility

scholarly journals Deficiency of Ku Induces Host Cell Exploitation in Human Cancer Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Okay Saydam ◽  
Nurten Saydam
Keyword(s):  
Host Cell ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Metastasis ◽  
Human Cancer ◽  
Therapy Resistance ◽  
Host Cells ◽  
Human Cancer Cells ◽  
Parasitic Lifestyle

Cancer metastasis is the major cause of death from cancer (Massague and Obenauf, 2016; Steeg, 2016). The extensive genetic heterogeneity and cellular plasticity of metastatic tumors set a prime barrier for the current cancer treatment protocols (Boumahdi and de Sauvage, 2020). In addition, acquired therapy resistance has become an insurmountable obstacle that abolishes the beneficial effects of numerous anti-cancer regimens (De Angelis et al., 2019; Boumahdi and de Sauvage, 2020). Here we report that deficiency of Ku leads to the exploitation of host cells in human cancer cell line models. We found that, upon conditional deletion of XRCC6 that codes for Ku70, HCT116 human colorectal cancer cells gain a parasitic lifestyle that is characterized by the continuous cycle of host cell exploitation. We also found that DAOY cells, a human medulloblastoma cell line, innately lack nuclear Ku70/Ku86 proteins and utilize the host-cell invasion/exit mechanism for maintenance of their survival, similarly to the Ku70 conditionally-null HCT116 cells. Our study demonstrates that a functional loss of Ku protein promotes an adaptive, opportunistic switch to a parasitic lifestyle in human cancer cells, providing evidence for a previously unknown mechanism of cell survival in response to severe genomic stress. We anticipate that our study will bring a new perspective for understanding the mechanisms of cancer cell evolution, leading to a shift in the current concepts of cancer therapy protocols directed to the prevention of cancer metastasis and therapy resistance.

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