Evidence map›Paper›PMID 32632148›Full record

ArticleBritish journal of cancer2020

IQGAP1 promotes anoikis resistance and metastasis through Rac1-dependent ROS accumulation and activation of Src/FAK signalling in hepatocellular carcinoma.

Chun-Fen Mo, Jun Li, Shu-Xia Yang, Hui-Jie Guo, Yang Liu, Xing-Yan Luo, Yan-Tang Wang, Min-Hui Li, Jing-Yi Li, Qiang Zou

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. 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 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Chun-Fen Mo *Department of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China. mochunfen@cmc.edu.cn.
Jun Li *Department of Gastroenterology, The first affiliated hospital of Chengdu medical college, Chengdu, China.
Shu-Xia Yang *Department of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China.
Hui-Jie GuoDepartment of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China.
Yang LiuDepartment of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China.
Xing-Yan LuoDepartment of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China.
Yan-Tang WangDepartment of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China.
Min-Hui LiDepartment of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China.
Jing-Yi LiDepartment of Urology, The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, China. lijingyi@cmc.edu.cn.
Qiang ZouDepartment of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China. qiangzou99@gmail.com.
Chengdu Medical College · CNFirst Affiliated Hospital of Chengdu Medical College · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81402944National Natural Science Foundation of China (National Science Foundation of China) 81871300
6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) has a crucial role in the progression of hepatocellular carcinoma (HCC). Tumour cells must develop anoikis resistance in order to survive before metastasis. This study aimed to investigate the mechanism of IQGAP1 in HBV-mediated anoikis evasion and metastasis in HCC cells.

methodsIQGAP1 expression was detected by immunohistochemistry, real-time PCR and immunoblot analysis. Lentiviral-mediated stable upregulation or knockdown of IGAQP1, immunoprecipitation, etc. were used in function and mechanism study.

resultsIQGAP1 was markedly upregulated in HBV-positive compared with HBV-negative HCC cells and tissues. IQGAP1 was positively correlated to poor prognosis of HBV-associated HCC patients. IQGAP1 overexpression significantly enhanced the anchorage-independent growth and metastasis, whereas IQGAP1-deficient HCC cells are more sensitive to anoikis. Mechanistically, we found that HBV-induced ROS enhanced the association of IQGAP1 and Rac1 that activated Rac1, leading to phosphorylation of Src/FAK pathway. Antioxidants efficiently inhibited IQGAP1-mediated anoikis resistance and metastasis.

conclusionsOur study indicated an important mechanism by which upregulated IQGAP1 by HBV promoted anoikis resistance, migration and invasion of HCC cells through Rac1-dependent ROS accumulation and activation of Src/FAK signalling, suggesting IQGAP1 as a prognostic indicator and a novel therapeutic target in HCC patients with HBV infection.

Indexed as

AnimalsAnoikisCarcinoma, HepatocellularCell Line, TumorFemaleFocal Adhesion Kinase 1Hepatitis BHumansLiver NeoplasmsMiceMice, Inbred BALB CNeoplasm Metastasisrac1 GTP-Binding Proteinras GTPase-Activating ProteinsReactive Oxygen SpeciesSignal TransductionFocal Adhesion Kinase 1IQ motif containing GTPase activating protein 1PTK2 protein, humanrac1 GTP-Binding ProteinRAC1 protein, humanras GTPase-Activating ProteinsReactive Oxygen Speciessrc-Family Kinases

Identifiers

PMID32632148
PMCPMC7525663
OpenAlexW4211256650

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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.