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Up-regulation of UVRAG by HDAC1 Inhibition Attenuates 5FU-induced Cell Death in HCT116 Colorectal Cancer Cells.

Abstract The ultraviolent irradiation resistance-associated gene (UVRAG), a component of the Beclin 1/autophagy-related 6 complex, regulates the autophagy initiation step and functions in the DNA-damage response. UVRAG is frequently mutated in various cancer types, and mutations of UVRAG increase sensitivity to chemotherapy by impairing DNA-damage repair. In this study, we addressed the epigenetic regulation of UVRAG in colorectal cancer cells. UVRAG expression was increased in cells treated with histone deacetylase (HDAC) inhibitors, such as valproic acid and suberoylanilide hydroxamic acid. Down-regulation of HDAC1 enhanced UVRAG expression in colorectal cancer cells. In addition, both chemical and genetic inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in 5-fluorouracil (5FU)-treated cancer cells. In contrast, UVRAG overexpression inhibited caspase activation and cell death in 5FU-treated cells. Taken together, our findings suggest that up-regulation of UVRAG by HDAC1 inhibition potentiates DNA-damage-mediated cell death in colorectal cancer cells.
PMID
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Authors

Mayor MeshTerms
Keywords

5FU

HDAC1

UVRAG

colorectal cancer

epigenetics

Journal Title anticancer research
Publication Year Start




PMID- 29277783
OWN - NLM
STAT- In-Process
LR  - 20171226
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 38
IP  - 1
DP  - 2018 Jan
TI  - Up-regulation of UVRAG by HDAC1 Inhibition Attenuates 5FU-induced Cell Death in
      HCT116 Colorectal Cancer Cells.
PG  - 271-277
AB  - The ultraviolent irradiation resistance-associated gene (UVRAG), a component of
      the Beclin 1/autophagy-related 6 complex, regulates the autophagy initiation step
      and functions in the DNA-damage response. UVRAG is frequently mutated in various 
      cancer types, and mutations of UVRAG increase sensitivity to chemotherapy by
      impairing DNA-damage repair. In this study, we addressed the epigenetic
      regulation of UVRAG in colorectal cancer cells. UVRAG expression was increased in
      cells treated with histone deacetylase (HDAC) inhibitors, such as valproic acid
      and suberoylanilide hydroxamic acid. Down-regulation of HDAC1 enhanced UVRAG
      expression in colorectal cancer cells. In addition, both chemical and genetic
      inhibition of HDAC1 reduced the activation of caspase-3 and cytotoxicity in
      5-fluorouracil (5FU)-treated cancer cells. In contrast, UVRAG overexpression
      inhibited caspase activation and cell death in 5FU-treated cells. Taken together,
      our findings suggest that up-regulation of UVRAG by HDAC1 inhibition potentiates 
      DNA-damage-mediated cell death in colorectal cancer cells.
CI  - Copyright(c) 2018, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Jo, Yoon Kyung
AU  - Jo YK
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea.
FAU - Park, Na Yeon
AU  - Park NY
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea.
FAU - Shin, Ji Hyun
AU  - Shin JH
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea.
FAU - Jo, Doo Sin
AU  - Jo DS
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea.
FAU - Bae, Ji-Eun
AU  - Bae JE
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea.
FAU - Choi, Eun Sun
AU  - Choi ES
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea.
FAU - Maeng, Sungho
AU  - Maeng S
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea.
FAU - Jeon, Hong Bae
AU  - Jeon HB
AD  - Biomedical Research Institute, MEDIPOST Corporation, Seongnam, Republic of Korea.
FAU - Roh, Seon Ae
AU  - Roh SA
AD  - Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea.
FAU - Chang, Jong Wook
AU  - Chang JW
AD  - Stem Cell & Regenerative Medicine Institute, Samsung Medical Center, Seoul,
      Republic of Korea.
FAU - Kim, Jin Cheon
AU  - Kim JC
AD  - Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea
      [email protected] [email protected]
AD  - Department of Surgery, University of Ulsan College of Medicine, Asan Medical
      Center, Seoul, Republic of Korea.
FAU - Cho, Dong-Hyung
AU  - Cho DH
AD  - Department of Gerontology, Graduate School of East-West Medical Science, Kyung
      Hee University, Seoul, Republic of Korea [email protected] [email protected]
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
OTO - NOTNLM
OT  - 5FU
OT  - HDAC1
OT  - UVRAG
OT  - colorectal cancer
OT  - epigenetics
EDAT- 2017/12/27 06:00
MHDA- 2017/12/27 06:00
CRDT- 2017/12/27 06:00
PHST- 2017/10/03 00:00 [received]
PHST- 2017/10/26 00:00 [revised]
PHST- 2017/10/31 00:00 [accepted]
PHST- 2017/12/27 06:00 [entrez]
PHST- 2017/12/27 06:00 [pubmed]
PHST- 2017/12/27 06:00 [medline]
AID - 38/1/271 [pii]
PST - ppublish
SO  - Anticancer Res. 2018 Jan;38(1):271-277.