Evidence map›Paper›PMID 31655604›Full record

ArticleJournal of translational medicine2019

CD36 promotes the epithelial-mesenchymal transition and metastasis in cervical cancer by interacting with TGF-β.

Min Deng, Xiaodong Cai, Ling Long, Linying Xie, Hongmei Ma, Youjian Zhou, Shuguang Liu, Chao Zeng

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
2.8field-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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Min DengAffliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, 510095, Guangdong, China.
Xiaodong CaiDepartment of Neurology, The Sixth Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510655, Guangdong, China.
Ling LongDepartment of Neurology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510600, Guangdong, China.
Linying XieDepartment of Pathology, The Eighth Affiliated Hospital, Sun Yat-sen University, Futian District, Shenzhen, 518033, Guangdong, China.
Hongmei MaDepartment of Pathology, The Eighth Affiliated Hospital, Sun Yat-sen University, Futian District, Shenzhen, 518033, Guangdong, China.
Youjian ZhouDepartment of Pathology, The Eighth Affiliated Hospital, Sun Yat-sen University, Futian District, Shenzhen, 518033, Guangdong, China.
Shuguang LiuDepartment of Pathology, The Eighth Affiliated Hospital, Sun Yat-sen University, Futian District, Shenzhen, 518033, Guangdong, China. SGL3016@163.com.
Chao ZengDepartment of Pathology, The Eighth Affiliated Hospital, Sun Yat-sen University, Futian District, Shenzhen, 518033, Guangdong, China. zengchaosysu@126.com.ORCID 0000-0001-5110-545X
Sun Yat-sen University · CNGuangzhou Medical University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulating evidence indicates that CD36 initiates metastasis and correlates with an unfavorable prognosis in cancers. However, there are few reports regarding the roles of CD36 in initiation and metastasis of cervical cancer.

methodsUsing immunohistochemistry, we analyzed 133 cervical cancer samples for CD36 protein expression levels, and then investigated the correlation between changes in its expression and clinicopathologic parameters. The effect of CD36 expression on the epithelial-mesenchymal transition (EMT) in cervical cancer cells was evaluated by Western immunoblotting analysis. In vitro invasion and in vivo metastasis assays were also used to evaluate the role of CD36 in cervical cancer metastasis.

resultsIn the present study, we confirmed that CD36 was highly expressed in cervical cancer samples relative to normal cervical tissues. Moreover, overexpression of CD36 promoted invasiveness and metastasis of cervical cancer cells in vitro and in vivo, while CD36 knockdown suppressed proliferation, migration, and invasiveness. We demonstrated that TGF-β treatment attenuated E-cadherin expression and enhanced the expression levels of CD36, vimentin, slug, snail, and twist in si-SiHa, si-HeLa, and C33a-CD36 cells, suggesting that TGF-β synergized with CD36 on EMT via active CD36 expression. We also observed that the expression levels of TGF-β in si-SiHa cells and si-HeLa cells were down-regulated, whereas the expression levels of TGF-β were up-regulated in C33a-CD36 cells. These results imply that CD36 and TGF-β interact with each other to promote the EMT in cervical cancer.

conclusionsOur findings suggest that CD36 is likely to be an effective target for guiding individualized clinical therapy of cervical cancer.

Indexed as

AnimalsApoptosisCD36 AntigensCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHeLa CellsHumansImmunohistochemistryKangai-1 ProteinMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessCD36 AntigensCD36 protein, humanCD82 protein, humanKangai-1 ProteinTransforming Growth Factor betaCD36Cervical cancerEMTMetastasisTGF-β

Identifiers

PMID31655604
PMCPMC6815430
OpenAlexW2982093765

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LicenceCC BY
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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.