pp4r1 accelerates cell growth and proliferation in hepg2 hepatocellular carcinoma
Clicks: 176
ID: 153637
2015
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Steady Performance
30.0
/100
176 views
31 readers
AI Quality Assessment
Not analyzed
Readership in this journal
SteadyRanked #131 of 171 articles by views in jurnal tam
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 171 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
Gang Wu, Zhenyu Ma, Jianmin Qian, Bin LiuDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, People’s Republic of ChinaAbstract: Hepatocellular carcinoma (HCC), as the fifth most common cancer worldwide, has become the third leading cause of cancer-related deaths. It is reported that protein phosphatase 4 (PP4) is an essential protein for nucleation, growth, and stabilization of microtubules in centrosomes/spindle bodies during cell division. Besides, previous studies have identified protein phosphatase 4 regulatory subunit 1 (PP4R1) as a constitutive interaction partner of PP4 catalytic subunit PP4C. The PP4C-PP4R1 PP4 complex plays a role in dephosphorylation, regulation of histone acetylation, and NF-κB activation. However, little is known about the pathological functions of PP4R1 in human cancers. Thus, in order to investigate how PP4R1 functions in human HCC, two common hepatocarcinogenesis HCC cell lines HepG2 and SMMC-7721 were employed, transduced with recombinant lentivirus expressing PP4R1 short hairpin RNA. Compared with the controls, the cells treated with Lv-shPP4R1 showed a significant decrease in cell proliferation and colony formation. The results of flow cytometry showed that the knockdown of PP4R1 caused HepG2 cells arrest at G2/M phase in the cell cycle. Furthermore, the transduction of Lv-shPP4R1 into HepG2 cells led to the inactivation of two major mitogen-activated protein kinase signaling cascades: p38 and c-Jun N-terminal kinase (JNK), indicating that PP4R1 could promote cell proliferation, which might be regulated by p38 and c-Jun N-terminal kinase pathways. In a word, this study highlights the crucial role of PP4R1 in promoting HCC cell growth, which might elucidate the pathological mechanism of HCC.Keywords: hepatocellular carcinoma, PP4R1, shRNA, proliferation, apoptosis
| Reference Key |
g2015oncotargetspp4r1
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | ;Wu G;Ma ZY;Qian JM;Liu B |
| Journal | jurnal tam |
| Year | 2015 |
| DOI |
DOI not found
|
| URL | |
| Keywords |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.