number of access : ?
number of downloads : ?
ID 115670
Author
Qi, Guangying Guilin Medical University|Prefectural University of Hiroshima
Tang, Bo Guilin Medical University
Liu, Tian Guilin Medical University
Jin, Shengjian Guilin Medical University
Liu, Jing Guilin Medical University
Zuo, Xiaoxu Guilin Medical University
Mi, Sisi Guilin Medical University
Shao, Wenhuan Guilin Medical University
Ma, Xiaojuan Guilin Medical University
Zeng, Sien Guilin Medical University
Tatsuka, Masaaki Prefectural University of Hiroshima
Shimamoto, Fumio Prefectural University of Hiroshima
Keywords
PARP6
Survivin
colorectal cancer
tumor suppressor
prognosis
Content Type
Journal Article
Description
Poly (ADP-ribose) polymerases (PARPs) are enzymes that transfer ADP-ribose groups to target proteins and are involved in a variety of biological processes. PARP6 is a novel member, and our previous findings suggest that PARP6 may act as a tumor suppressor via suppressing cell cycle progression. However, it is still unclear that PARP6 function besides growth suppression in colorectal cancer (CRC). In this study, we examined tumor suppressive roles of PAPR6 in CRC cells both in vitro and in vivo. We found that PARP6 inhibited colony formation, invasion and migration as well as cell proliferation. Moreover, ectopic overexpression of PARP6 decreased Survivin expression, which acts as an oncogene and is involved in apoptosis and mitosis. We confirmed the inverse correlation between PARP6 and Survivin expression in CRC cases by immunohistochemistry. Importantly, CRC cases with downregulation of PARP6 and upregulation of Survivin showed poor prognosis. In summary, PARP6 acts as a tumor suppressor via downregulating Survivin expression in CRC. PARP6 can be a novel diagnostic and therapeutic target together with Survivin for CRC.
Journal Title
Oncotarget
ISSN
19492553
Publisher
Impact Journals
Volume
7
Issue
14
Start Page
18812
End Page
18824
Published Date
2016-02-25
Rights
This is licensed under a Creative Commons Attribution 3.0 License(https://creativecommons.org/licenses/by/3.0/).
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Oral Sciences