Evidence map›Paper›PMID 32746865›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

COL4A1 promotes the growth and metastasis of hepatocellular carcinoma cells by activating FAK-Src signaling.

Ting Wang, Haojie Jin, Jingying Hu, Xi Li, Haoyu Ruan, Huili Xu, Lin Wei, Weihua Dong, Fei Teng, Jianren Gu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
12.9field-weighted citation impact, top 1% 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

85 citing papers in PubMed, 150 citations in OpenAlex.

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25 more citing papers are in PubMed but not listed here.

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

13 authors at 7 institutions in 1 country.

Ting WangShanghai Medical College of Fudan University, Shanghai, 200032, People's Republic of China.
Haojie JinState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200240, People's Republic of China.
Jingying HuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200240, People's Republic of China.
Xi LiThe Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, People's Republic of China.
Haoyu RuanShanghai Medical College of Fudan University, Shanghai, 200032, People's Republic of China.
Huili XuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200240, People's Republic of China.
Lin WeiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200240, People's Republic of China.
Weihua DongChangzheng Hospital, Navy Medical University, Shanghai, 200003, People's Republic of China.
Fei TengChangzheng Hospital, Navy Medical University, Shanghai, 200003, People's Republic of China.
Jianren GuShanghai Medical College of Fudan University, Shanghai, 200032, People's Republic of China.
Wenxin QinState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200240, People's Republic of China.
Xiaoying LuoState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200240, People's Republic of China. luoxy@shsci.org.
Yujun HaoState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200240, People's Republic of China. yjhao@shsci.org.
Shanghai Cancer Institute · CNRenji Hospital · CNShanghai Changzheng Hospital · CNShanghai Jiao Tong University · CNShanghai Medical College of Fudan University · CNState Key Laboratory of Oncogene and Related Genes · CNSun Yat-sen University · CN

Funding

Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning TP2017027Shanghai Municipal Commission of Health and Family Planning 201640261Shanghai Municipal Commission of Health and Family Planning 20194Y0248Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support 20171915State Key Laboratory of Oncogenes and Related Genes SB19-05the Program of Shanghai Academic/Technology Research Leader 19XD1423500
6 · The paper itself

Abstract

backgroundCollagens are the most abundant proteins in extra cellular matrix and important components of tumor microenvironment. Recent studies have showed that aberrant expression of collagens can influence tumor cell behaviors. However, their roles in hepatocellular carcinoma (HCC) are poorly understood.

methodsIn this study, we screened all 44 collagen members in HCC using whole transcriptome sequencing data from the public datasets, and collagen type IV alpha1 chain (COL4A1) was identified as most significantly differential expressed gene. Expression of COL4A1 was detected in HCC samples by quantitative real-time polymerase chain reaction (qRT-PCR), western blot and immunohistochemistry (IHC). Finally, functions and potential mechanisms of COL4A1 were explored in HCC progression.

resultsCOL4A1 is the most significantly overexpressed collagen gene in HCC. Upregulation of COL4A1 facilitates the proliferation, migration and invasion of HCC cells through FAK-Src signaling. Expression of COL4A1 is upregulated by RUNX1 in HCC. HCC cells with high COL4A1 expression are sensitive to the treatment with FAK or Src inhibitor.

conclusionCOL4A1 facilitates growth and metastasis in HCC via activation of FAK-Src signaling. High level of COL4A1 may be a potential biomarker for diagnosis and treatment with FAK or Src inhibitor for HCC.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCarcinoma, HepatocellularCase-Control StudiesCell MovementCell ProliferationCollagen Type IVFemaleFocal Adhesion Kinase 1HumansLiver NeoplasmsMiceMice, NudeNeoplasm InvasivenessBiomarkers, TumorCOL4A1 protein, humanCollagen Type IVFocal Adhesion Kinase 1PTK2 protein, humansrc-Family KinasesCOL4A1FAKHCCRUNX1Src

Identifiers

PMID32746865
PMCPMC7398077
OpenAlexW3047409550

What Socratic 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 Socratic graph.