Elevation of CD109 promotes metastasis and drug resistance in lung cancer via activation of EGFR-AKT-mTOR signaling

Cancer Science
Kang-Yun LeeCheng-Wei Lin

Abstract

Lung cancer is the most commonly diagnosed cancer worldwide, and metastasis in lung cancer is the leading cause of cancer-related deaths. Thus, understanding the mechanism of lung cancer metastasis will improve the diagnosis and treatment of lung cancer patients. Herein, we found that expression of cluster of differentiation 109 (CD109) was correlated with the invasive and metastatic capacities of lung adenocarcinoma cells. CD109 is upregulated in tumorous tissues, and CD109 overexpression was associated with tumor progression, distant metastasis, and a poor prognosis in patient with lung adenocarcinoma. Mechanistically, expression of CD109 regulates protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling via its association with the epidermal growth factor receptor (EGFR). Inhibition of CD109 decreases EGFR phosphorylation, diminishes EGF-elicited activation of AKT/mTOR, and sensitizes tumor cells to an EGFR inhibitor. Taken together, our results show that CD109 is a potential diagnostic and therapeutic target in lung cancer patients.

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Citations

Jun 3, 2021·International Journal of Molecular Sciences·Yi-Chun ChaoCheng-Wei Lin
Nov 12, 2021·Virchows Archiv : an International Journal of Pathology·Kai AdachiYoshiki Murakumo

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Methods Mentioned

BETA
electrophoresis
PCR
protein kinase array

Software Mentioned

Xena
GraphPad Prism
GenePrint
GSEA

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