Evidence map›Paper›PMID 31920339›Full record

ArticleOncoTargets and therapy2019

ARHGAP10 Inhibits the Proliferation and Metastasis of CRC Cells via Blocking the Activity of RhoA/AKT Signaling Pathway.

Lin Liu, Dongyu Xie, Haina Xie, Wei Huang, Jingxian Zhang, Wenye Jin, Wenjing Jiang, Donghao Xie

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 65 citations in OpenAlex.

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  9. ZNF197-AS1/miR-425/GABARAPL1 axis: a novel regulatory mechanism in uveal melanoma.American journal of physiology. Cell physiology · 2024
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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

8 authors at 5 institutions in 1 country.

Lin Liu *Department of Pharmacy, Dahua Hospital, Shanghai, People's Republic of China.
Dongyu Xie *Department of Spleen-Stomach, Zhenjiang Affiliated Hospital of Nanjing University of Chinese Medicine, Zhenjiang, People's Republic of China.
Haina Xie *School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Wei HuangDepartment of Pharmacy, Dahua Hospital, Shanghai, People's Republic of China.
Jingxian ZhangDepartment of Pharmacy, Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, People's Republic of China.
Wenye JinDepartment of Pharmacy, Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, People's Republic of China.
Wenjing JiangDepartment of Pharmacy, Dahua Hospital, Shanghai, People's Republic of China.
Donghao XieDepartment of Pharmacy, Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, People's Republic of China.
Dahua Hospital · CNShanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine · CNJiangsu University · CNNanjing University of Chinese Medicine · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionARHGAP10 belongs to the ARHGAP family, which is downregulated in certain human tumors. However, the detailed function of ARHGAP10 remains unclear in human colon carcinoma (CRC). In the current study, we aimed to explore the role of ARHGAP10 in the growth and metastasis of CRC cells.

methodsARHGAP10 was induced silencing and overexpression using RNA interference (RNAi) and lentiviral-vector in CRC cells. Quantitative real-time PCR (qRT-PCR) and Western blot were used to quantify the mRNA and protein contents of ARHGAP10. Cell proliferation was determined by using Cell counting kit-8 (CCK-8). Transwell assay was utilized to examine the role of ARHGAP10 in the migration and invasion of CRC cells.

resultsOur results indicated that ARHGAP10 was downregulated in human CRC tissues and low expression of ARHGAP10 was associated with poor prognosis of patients with CRC. Moreover, ARHGAP10 overexpression significantly inhibited the proliferation and metastasis of CRC cells. Moreover, a PI3K/AKT inhibitor LY294002 was utilized to examine the connection between ARHGAP10 and AKT. Our findings demonstrated that the AKT inhibitor LY294002 could rescue the function of ARHGAP10 in CRC cells. DISCUSSION: It was the first time to elucidate that AKT involved in the ARHGAP10 signaling pathway and ARHGAP10 negatively mediated the phosphorylation of AKT (p-AKT) and RhoA activity in CRC cells. Interestingly, the Rho/MRTF/SRF inhibitor CCG-1423 significantly inhibited the phosphorylation of AKT in ARHGAP10 siRNA transfected CRC cells. Much importantly, overexpression of ARHGAP10 deeply suppressed the metastasis of CRC cells in the lung in vivo. Taken together, our findings not only enhanced the understanding of the anti-cancer effect of ARHGAP10 in CRC cells but also indicated its underlying pathway in CRC.

Indexed as

AKTARHGAP10colon carcinomaRhoA activity

Identifiers

PMID31920339
PMCPMC6938210
OpenAlexW2997956862

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.