https://scholars.lib.ntu.edu.tw/handle/123456789/557695
標題: | CD73 Is regulated by the EGFR-ERK signaling pathway in non-small cell lung cancer | 作者: | Griesing S. BIN-CHI LIAO CHIH-HSIN YANG |
公開日期: | 2021 | 出版社: | International Institute of Anticancer Research | 卷: | 41 | 期: | 3 | 起(迄)頁: | 1231-1242 | 來源出版物: | Anticancer Research | 摘要: | Background/Aim: Successful therapy of EGFR-mutant NSCLC remains a challenging task despite initial benefits with the usage of EGFR tyrosine kinase inhibitors. Cancer immunotherapy has shown promising results in certain tumors, but response rate in EGFR-mutant NCLC is low, because these tumors are thought to have weak immunogenicity. Materials and Methods: We used data from in vivo NSCLC databases as well as from in vitro cell culture experiments to investigate the regulation of CD73 by EGFR. Results: EGFR expression was correlated with CD73 expression in patients' datasets, with EGFR-mutant tumors showing higher expression than their EGFR wildtype counterparts. Treatment of EGFR-mutant NSCLC cell lines with EGFR TKI reduced expression of CD73 at both mRNA and protein level. Among EGFR downstream signaling pathways, the Ras-Raf-ERK pathway was involved in the regulation of CD73 expression directly via ERK1/2 without the engagement of RSKs or MSKs. Conclusion: The results of this study may provide novel therapeutic strategies for the treatment of oncogene-driven NSCLC. ? 2021 International Institute of Anticancer Research. All rights reserved. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85103205640&doi=10.21873%2fANTICANRES.14880&partnerID=40&md5=1f7da64aa6f82ca33a3050e45f354662 https://scholars.lib.ntu.edu.tw/handle/123456789/557695 |
ISSN: | 0250-7005 | DOI: | 10.21873/anticanres.14880 | SDG/關鍵字: | 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene; 5' nucleotidase; 8 [4 (1 aminocyclobutyl)phenyl] 9 phenyl 1,2,4 triazolo[3,4 f][1,6]naphthyridin 3(2h) one; afatinib; epidermal growth factor receptor; epidermal growth factor receptor kinase inhibitor; gefitinib; ljh 685; ljh685; messenger RNA; mitogen activated protein kinase 1; mitogen activated protein kinase 3; osimertinib; ravoxertinib; ruxolitinib; sb 747641a; sb747641a; selumetinib; ulixertinib; unclassified drug; 5' nucleotidase; EGFR protein, human; epidermal growth factor receptor; glycosylphosphatidylinositol anchored protein; mitogen activated protein kinase; NT5E protein, human; adult; Article; cell culture; cell viability; controlled study; data analysis software; data base; HCC827 cell line; human; human cell; in vitro study; in vivo study; MAPK signaling; mRNA expression level; NCI-H441 cell line; non small cell lung cancer; oncogene; priority journal; protein expression; protein expression level; regulatory mechanism; wild type; gene expression regulation; genetics; lung tumor; non small cell lung cancer; pathophysiology; physiology; signal transduction; tumor cell line; 5'-Nucleotidase; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; ErbB Receptors; Extracellular Signal-Regulated MAP Kinases; Gene Expression Regulation, Neoplastic; GPI-Linked Proteins; Humans; Lung Neoplasms; MAP Kinase Signaling System; Signal Transduction |
顯示於: | 腫瘤醫學研究所 |
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