Loss of EGF-dependent cell proliferation ability on radioresistant cell HepG2-8960-R

Yohei Saito; Ryo Abiko; Akira Kishida; Yoshikazu Kuwahara; Yumi Yamamoto; Fumihiko Yamamoto; Manabu Fukumoto; Yasuhito Ohkubo

doi:10.1002/cbf.3090

Loss of EGF-dependent cell proliferation ability on radioresistant cell HepG2-8960-R

Yohei Saito, Ryo Abiko, Akira Kishida, Yoshikazu Kuwahara, Yumi Yamamoto, Fumihiko Yamamoto, Manabu Fukumoto, Yasuhito Ohkubo

Division of Cancer Science

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	73-79
Number of pages	7
Journal	Cell Biochemistry and Function
Volume	33
Issue number	2
DOIs	https://doi.org/10.1002/cbf.3090
Publication status	Published - 2015 Mar 1

Keywords

Cetuximab
Hepatocellular carcinoma
Radiation
Radioresistance

ASJC Scopus subject areas

Biochemistry
Clinical Biochemistry
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1002/cbf.3090

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title = "Loss of EGF-dependent cell proliferation ability on radioresistant cell HepG2-8960-R",

abstract = "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.",

keywords = "Cetuximab, Hepatocellular carcinoma, Radiation, Radioresistance",

author = "Yohei Saito and Ryo Abiko and Akira Kishida and Yoshikazu Kuwahara and Yumi Yamamoto and Fumihiko Yamamoto and Manabu Fukumoto and Yasuhito Ohkubo",

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year = "2015",

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doi = "10.1002/cbf.3090",

language = "English",

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T1 - Loss of EGF-dependent cell proliferation ability on radioresistant cell HepG2-8960-R

AU - Saito, Yohei

AU - Abiko, Ryo

AU - Kishida, Akira

AU - Kuwahara, Yoshikazu

AU - Yamamoto, Yumi

AU - Yamamoto, Fumihiko

AU - Fukumoto, Manabu

AU - Ohkubo, Yasuhito

PY - 2015/3/1

Y1 - 2015/3/1

N2 - 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.

AB - 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.

KW - Cetuximab

KW - Hepatocellular carcinoma

KW - Radiation

KW - Radioresistance

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JO - Cell Biochemistry and Function

JF - Cell Biochemistry and Function

SN - 0263-6484

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ER -

Loss of EGF-dependent cell proliferation ability on radioresistant cell HepG2-8960-R

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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