Evidence map›Paper›PMID 28375585›Full record

ArticleCancer science2017

Downregulation of Talin1 promotes hepatocellular carcinoma progression through activation of the ERK1/2 pathway.

Peijuan Chen, Ling Lei, Jian Wang, Xuejing Zou, Dongyan Zhang, Ling Deng, Dehua Wu

Abstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. Weak and Tunable Adhesion-Clutch Drives Rapid Cell Migration and Glioblastoma Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  9. Prognostic value of Talin-1 in renal cell carcinoma and its association with B7-H3.Cancer biomarkers : section A of Disease markers · 2022
    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

7 authors.

Peijuan ChenDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ling LeiDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jian WangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xuejing ZouHepatology Unit and Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Dongyan ZhangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ling DengDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Dehua WuDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0001-9172-1118

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Talin1 is an adaptor protein that conjugates integrins to the cytoskeleton and regulates integrins and focal adhesion signaling. Several studies have found that Talin1 is overexpressed in several tumor types and promotes tumor progression. However, the explicit role of Talin1 in hepatocellular carcinoma (HCC) progression is still unclear and its functional mechanism remains largely unknown. In this study, we showed a trend of gradually decreasing expression of Talin1 from normal liver tissues to hepatocirrhosis, liver hyperplasia, the corresponding adjacent non-tumor, primary HCC, and eventually metastatic foci, indicating that Talin1 may correlate with HCC initiation to progression. Talin1 was significantly downregulated in HCC tissues compared with adjacent non-tumor tissues and low Talin1 expression was associated with HCC progression and poor prognosis. Furthermore, Talin1 knockdown induced epithelial-mesenchymal transition and promoted migration and invasion in SK-Hep-1 cells and HepG2 cells. Mechanistically, we found that the ERK pathway was responsible for these promoting effects of Talin1 knockdown in HCC cells. The promoting effects of Talin1 knockdown on epithelial-mesenchymal transition, migration, and invasion were reversed by U0126, a specific ERK1/2 inhibitor. Taken together, our results suggested that Talin1 might serve as a tumor suppressor in HCC and a potential prognostic biomarker for HCC patients.

Indexed as

Carcinoma, HepatocellularCell LineCell Line, TumorCell MovementDisease ProgressionDown-RegulationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMaleMAP Kinase Signaling SystemMiddle AgedSignal TransductionTalinTLN1 protein, humanEpithelial-mesenchymal transitionERK1/2 pathwayhepatocellular carcinomaprognostic biomarkerTalin1

Identifiers

PMID28375585
PMCPMC5480078

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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.