Loss of EGF‐dependent cell proliferation ability on radioresistant cell HepG2‐8960‐R. (6th February 2015)

• Record Type: Journal Article
• Authors: Saito, Yohei; Abiko, Ryo; Kishida, Akira; Kuwahara, Yoshikazu; Yamamoto, Yumi; Yamamoto, Fumihiko; Fukumoto, Manabu; Ohkubo, Yasuhito
• Is Part Of: Cell biochemistry and function. Volume 33:Number 2(2015:Mar.)
• Page Start: 73
• Page End: 79
• Publication Date: 2015-02-06
• Subjects: Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3090
• Languages: English
• ISSNs: 0263-6484

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>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 &amp; Sons, Ltd.</p> </abstract>