Evidence map›Paper›PMID 27010858›Full record

ArticleCell death & disease2016

ARHGAP10, downregulated in ovarian cancer, suppresses tumorigenicity of ovarian cancer cells.

N Luo, J Guo, L Chen, W Yang, X Qu, Z Cheng

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 68 citations in OpenAlex.

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  11. miR-21-5p serves as a promoter in renal cell carcinoma progression through ARHGAP24 downregulation.Environmental science and pollution research international · 2022
    Article
  12. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
  13. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

N LuoDepartment of Gynecology & Obstetrics, Yangpu Hospital, School of Medicine, Tongji University, Shanghai 200090, China.
J GuoDepartment of Gynecology & Obstetrics, Yangpu Hospital, School of Medicine, Tongji University, Shanghai 200090, China.
L ChenDepartment of Gynecology & Obstetrics, Yangpu Hospital, School of Medicine, Tongji University, Shanghai 200090, China.
W YangDepartment of Gynecology & Obstetrics, Yangpu Hospital, School of Medicine, Tongji University, Shanghai 200090, China.
X QuDepartment of Gynecology & Obstetrics, Yangpu Hospital, School of Medicine, Tongji University, Shanghai 200090, China.
Z ChengDepartment of Gynecology & Obstetrics, Yangpu Hospital, School of Medicine, Tongji University, Shanghai 200090, China.
Tongji University · CNYangpu Hospital of Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rho GTPase-activating proteins (RhoGAPs) are implicated in the development and progression of ovarian cancer. ARHGAP10 is a member of RhoGAP proteins and inactivates Cdc42 by converting GTP-bound form to GDP-bound form. Here, we aimed to evaluate ARHGAP10 expression profile and functions in ovarian cancer. The decreased expression of ARHGAP10 was found in 77.3% (58/75) of ovarian cancer tissues, compared with their non-tumorous counterparts. Furthermore, overall survival in ovarian cancer patients with higher expression of ARHGAP10 was longer than those with lower expression. Ectopic expression of ARHGAP10 in two ovarian cancer cell lines with lower expression of ARHGAP10 (A2780 and HO-8910) dramatically suppressed cell proliferation in vitro. In nude mice, its stable overexpression significantly inhibited the tumorigenicity of A2780 cells. We further demonstrated that overexpression of ARHGAP10 significantly inhibited cell adhesion, migration and invasion, resulted in cell arrest in G1 phase of cell cycle and a significant increase of apoptosis. Moreover, ARHGAP10 interacted with Cdc42 and overexpression of ARHGAP10 inhibited the activity of Cdc42 in A2780 cells. Gene set enrichment analysis on The Cancer Genome Atlas dataset showed that KEGG cell cycle, replication and base excision repair (BER) pathways were correlatively with the ARHGAP10 expression, which was further confirmed in ovarian cancer cells by western blotting. Hence, ARHGAP10 may serve as a tumor suppressor through inactivating Cdc42, as well as inhibiting cell cycle, replication and BER pathways. Our data suggest an important role of ARHGAP10 in the molecular etiology of cancer and implicate the potential application of ARHGAP10 in cancer therapy.

Indexed as

Down-RegulationGene Expression Regulation, NeoplasticSignal TransductionAnimalscdc42 GTP-Binding ProteinFemaleGTPase-Activating ProteinsHumansMiceOvarian NeoplasmsrhoA GTP-Binding ProteinTumor Suppressor ProteinsARHGAP10 protein, humanArhgap10 protein, mousecdc42 GTP-Binding ProteinCdc42 protein, mouseGTPase-Activating ProteinsrhoA GTP-Binding ProteinTumor Suppressor Proteins

Identifiers

PMID27010858
PMCPMC4823924
OpenAlexW2304437938

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.