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

• DOI: 10.1111/cas.14373
• Publication Date: 2020-03-05T07:19:40Z
• Authors: Kang‐Yun Lee; Pei‐Wei Shueng; Chih‐Ming Chou; Bo‐Xing Lin; Mei‐Hsiang Lin; Deng‐Yu Kuo; I‐Lin Tsai; Sheng‐Ming Wu; Cheng‐Wei Lin
• Keywords: Targeted Therapy

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