Evidence map›Paper›PMID 28969700›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

Kindlin-2 promotes hepatocellular carcinoma invasion and metastasis by increasing Wnt/β-catenin signaling.

Jie Lin, Wansong Lin, Yunbin Ye, Liping Wang, Xiaoyan Chen, Shengbing Zang, Aimin Huang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Jie LinDepartment of Pathology, The School of Basic Medical Sciences, Fujian Medical University, No.1, Xuefu North Road, University Town, Fuzhou, 350122, Fujian, China.
Wansong LinLaboratory of Immuno-Oncology, Fujian Cancer Hospital and Fujian Medical University Cancer hospital, Fuzhou, 350014, China.
Yunbin YeLaboratory of Immuno-Oncology, Fujian Cancer Hospital and Fujian Medical University Cancer hospital, Fuzhou, 350014, China.
Liping WangDepartment of Pathology, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Xiaoyan ChenDepartment of Pathology, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China.
Shengbing ZangDepartment of Pathology, The School of Basic Medical Sciences, Fujian Medical University, No.1, Xuefu North Road, University Town, Fuzhou, 350122, Fujian, China.
Aimin HuangDepartment of Pathology, The School of Basic Medical Sciences, Fujian Medical University, No.1, Xuefu North Road, University Town, Fuzhou, 350122, Fujian, China. draimin@163.com.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKindlin-2 is a member of the focal adhesion protein family that regulates invasion and metastasis in multiple malignancies; however, little is known about the role of Kindlin-2 in hepatocellular carcinoma (HCC) progression.

methodsImmunohistochemistry was used to investigate Kindlin-2 expression in 177 pairs of human HCC and adjacent liver tissue samples. The role of Kindlin-2 in the in vitro invasion and migration of HCC cell lines was evaluated in MHCC97H, LM3 and SMMC7721 cells. Microarray expression analysis was applied to explore the molecular mechanism through which Kindlin-2 promoted HCC progression. Quantitative real-time PCR and Western blotting were performed to verify the microarray results.

resultsHigh Kindlin-2 expression was found to significantly correlate with aggressive HCC clinicopathological features including tumor encapsulation, microvascular invasion, extrahepatic metastasis and poor prognosis. In vitro, Kindlin-2 knockout or knockdown inhibited HCC cell adhesion, migration and invasion, while ectopic Kindlin-2 expression promoted these processes. Importantly, Kindlin-2 activated Wnt/β-catenin signaling and increased β-catenin expression, especially levels of non-phosphorylated β-catenin, as well as two Wnt/β-catenin signaling pathway targets, Axin2 and MMP7. Kindlin-2 also induced a change in the expression profile of HCC cells, suggesting the cells underwent epithelial-mesenchymal transition. For example, the expression of the epithelial marker E-cadherin was downregulated, while the mesenchymal markers Vimentin, N-cadherin and Snail were upregulated.

conclusionKindlin-2 promotes HCC invasion, metastasis and epithelial-mesenchymal transition through Wnt/β-catenin signaling.

Indexed as

Up-RegulationWnt Signaling PathwayAgedCarcinoma, HepatocellularCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMaleMembrane ProteinsMiddle AgedNeoplasm InvasivenessFERMT2 protein, humanMembrane ProteinsNeoplasm ProteinsHepatocellular carcinomaInvasionKindlin-2MetastasisWnt/β-catenin signaling

Identifiers

PMID28969700
PMCPMC5623973
OpenAlexW2757119252

What OpenQuestion holds

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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.