Literature DB >> 26870184

Knockdown of protein phosphatase 5 inhibits ovarian cancer growth in vitro.

Xiaojiao Zheng1, Lianxiao Zhang1, Bohong Jin1, Fubin Zhang1, Duoyi Zhang1, Lining Cui1.   

Abstract

Ovarian cancer is the most common cause of gynecological cancer-related mortality. Serine/threonine protein phosphatase 5 (PP5, PPP5C) has been recognized to be involved in the regulation of multiple cellular signaling cascades that control diverse cellular processes, including cell growth, differentiation, proliferation, motility and apoptosis. In this study, to evaluate the functional role of PP5 in ovarian cancer cells, lentivirus-mediated RNA interference (RNAi) was applied to silence PPP5C in the human ovarian cancer cell line CAOV-3. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell colony forming ability was measured by colony formation. Cell cycle progression was determined by propidium iodide staining and flow cytometry. The results demonstrated that lentivirus-mediated RNAi specifically suppressed the expression of PPP5C at the mRNA and protein levels in CAOV-3 cells. Further investigations revealed that PP5 knockdown significantly inhibited the proliferation and colony formation of CAOV-3 cells. Moreover, the cell cycle of CAOV-3 cells was arrested at the G0/G1 phase following PP5 knockdown. This study highlights the crucial role of PP5 in promoting ovarian cancer cell proliferation, and provides a foundation for further study into the clinical potential of lentiviral-mediated delivery of PP5 RNAi therapy for the treatment of ovarian cancer.

Entities:  

Keywords:  RNA interference; lentivirus; ovarian cancer; proliferation; protein phosphatase 5

Year:  2015        PMID: 26870184      PMCID: PMC4727206          DOI: 10.3892/ol.2015.3828

Source DB:  PubMed          Journal:  Oncol Lett        ISSN: 1792-1074            Impact factor:   2.967


  26 in total

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7.  The molecular chaperone Hsp70 activates protein phosphatase 5 (PP5) by binding the tetratricopeptide repeat (TPR) domain.

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9.  Identification of a functional link for the p53 tumor suppressor protein in dexamethasone-induced growth suppression.

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10.  Synergistic effects of combined platelet-activating factor receptor and epidermal growth factor receptor targeting in ovarian cancer cells.

Authors:  Yi Yu; Mingxing Zhang; Xiaoyan Zhang; Qingqing Cai; Shanshan Hong; Wei Jiang; Congjian Xu
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  5 in total

1.  The Antitumor Drug LB-100 Is a Catalytic Inhibitor of Protein Phosphatase 2A (PPP2CA) and 5 (PPP5C) Coordinating with the Active-Site Catalytic Metals in PPP5C.

Authors:  Brandon M D'Arcy; Mark R Swingle; Cinta M Papke; Kevin A Abney; Erin S Bouska; Aishwarya Prakash; Richard E Honkanen
Journal:  Mol Cancer Ther       Date:  2019-01-24       Impact factor: 6.261

2.  Knockdown of serine/threonine protein phosphatase 5 enhances gemcitabine sensitivity by promoting apoptosis in pancreatic cancer cells in vitro.

Authors:  Jinhui Zhu; Yun Ji; Yuanquan Yu; Yun Jin; Xiaoxiao Zhang; Jiale Zhou; Yan Chen
Journal:  Oncol Lett       Date:  2018-03-28       Impact factor: 2.967

Review 3.  Structure and function of the co-chaperone protein phosphatase 5 in cancer.

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Journal:  Cell Stress Chaperones       Date:  2020-04-02       Impact factor: 3.667

4.  MiR-520a-5p/PPP5C regulation pattern is identified as the key to gemcitabine resistance in pancreatic cancer.

Authors:  Ruibiao Fu; Qian Shao; Bin Yang; Yan Chen; Qinghuang Ye; Xi Chen; Jinhui Zhu
Journal:  Front Oncol       Date:  2022-07-25       Impact factor: 5.738

5.  PPP5C promotes cell proliferation and survival in human prostate cancer by regulating of the JNK and ERK1/2 phosphorylation.

Authors:  Jian-Min Lv; Lu Chen; Yi Gao; Hai Huang; Xiu-Wu Pan; Xi Liu; Ming Chen; Fa-Jun Qu; Lin Li; Jun-Kai Wang; Xin-Gang Cui; Dan-Feng Xu
Journal:  Onco Targets Ther       Date:  2018-09-12       Impact factor: 4.147

  5 in total

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