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Loss of EGF‐dependent cell proliferation ability on radioresistant cell HepG2‐8960‐R
Author(s) -
Saito Yohei,
Abiko Ryo,
Kishida Akira,
Kuwahara Yoshikazu,
Yamamoto Yumi,
Yamamoto Fumihiko,
Fukumoto Manabu,
Ohkubo Yasuhito
Publication year - 2015
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3090
Subject(s) - radioresistance , cetuximab , cell growth , cancer research , epidermal growth factor receptor , epidermal growth factor , cell , cell culture , cancer , biology , chemistry , colorectal cancer , biochemistry , genetics
Acquired radioresistance of cancer cells interferes with radiotherapy and increases the probability of cancer recurrence. HepG2‐8960‐R, which is one of several clinically relevant radioresistant (CRR) cell lines, has a high tolerance to the repeated clinically relevant doses of X‐ray radiation. In this study, HepG2‐8960‐R had slightly lower cell proliferation ability than HepG2 in the presence of FBS. In particular, epidermal growth factor (EGF) hardly enhanced cell proliferation and DNA synthesis in HepG2‐8960‐R. Additionally, EGF could not induce the activation of Erk1/2, because the expression of EGF receptor (EGFR) protein decreased in HepG2‐8960‐R in accordance with the methylation of the EGFR promoter region. Therefore, cetuximab did not inhibit HepG2‐8960‐R cell proliferation. Our study showed that HepG2‐8960‐R had radioresistant and cetuximab‐resistant abilities. Copyright © 2015 John Wiley & Sons, Ltd.