Evidence map›Paper›PMID 29936709›Full record

ArticleCancer medicine2018

ARHGAP42 promotes cell migration and invasion involving PI3K/Akt signaling pathway in nasopharyngeal carcinoma.

Qian Hu, Xiao Lin, Linxiaoxiao Ding, Yinduo Zeng, Danmei Pang, Nengtai Ouyang, Yanqun Xiang, Herui Yao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

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  7. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Qian HuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, China.
Xiao LinGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, China.
Linxiaoxiao DingGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, China.
Yinduo ZengGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, China.
Danmei PangDepartment of Breast Cancer Oncology, Foshan Hospital of Sun Yat-Sen University, Foshan, China.
Nengtai OuyangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, China.
Yanqun XiangDepartment of Nasopharyngeal Carcinoma, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Herui YaoGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, China.ORCID 0000-0002-7398-2717
Sun Yat-sen University · CNFoshan Hospital of TCM · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rho GTPase-activating protein 42 was identified as an inhibitor of RhoA to maintain normal blood pressure homeostasis. However, the effect of ARHGAP42 in promoting cell malignancy in nasopharyngeal carcinoma is demonstrated in this study. Microarray and real-time quantitative PCR were used for a mRNA profiling of ARHGAP42 in nasopharyngeal primary and metastatic carcinoma tissues. Western blot and immunohistochemical staining were used for detecting the expression of ARHGAP42 protein in nasopharyngeal carcinoma tissues and cell lines. The overexpression and silence experiments of ARHGAP42 were performed in NPC cell lines using siRNA and expressive plasmid for evaluating cancer cell migration and invasion in vitro. Real-time quantitative PCR, western blot, and transwell test were employed for with the function of ARHGAP42 and its antisense lncRNA uc010rul. We confirmed the elevated expression of ARHGAP42 in metastatic NPC tissues of mRNA and protein for the first time. Immunohistochemical analysis indicated that NPC patients with highly ARHGAP42 expression were significantly associated with shorter metastasis-free survival. Knockdown of ARHGAP42 resulted in significant inhibition of nasopharyngeal cancer cell migration and invasion in vitro, and the overexpression of ARHGAP42 showed the opposite effects. In addition, the silence of uc010rul resulted in ARHGAP42 expression decrease and significant inhibition of nasopharyngeal cancer cell migration and invasion. High expression of ARHGAP42 is associated with poor metastasis-free survival of nasopharyngeal carcinoma patients. ARHGAP42 promotes migration and invasion of nasopharyngeal carcinoma cells in vitro; the antisense lncRNA may be involved in this effect.

Indexed as

Signal TransductionAdultAgedBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHumansMaleMiddle AgedNasopharyngeal NeoplasmsNeoplasm StagingARHGAP42 protein, humanBiomarkers, TumorGTPase-Activating ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, MessengerRNA, Small InterferingARHGAP42metastasisnasopharyngeal carcinomauc010rul

Identifiers

PMID29936709
PMCPMC6089169
OpenAlexW2810040068

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.