Evidence map›Paper›PMID 32059473›Full record

ArticleCancers2020

MAL2-Induced Actin-Based Protrusion Formation is Anti-Oncogenic in Hepatocellular Carcinoma.

Alfonso López-Coral, Gianna-Jade Del Vecchio, Joeffrey J Chahine, Bhaskar V Kallakury, Pamela L Tuma

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

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  4. Integration of multiomics analyses reveals unique insights into CD24-mediated immunosuppressive tumor microenvironment of breast cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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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

5 authors at 2 institutions in 1 country.

Alfonso López-CoralDepartment of Biology, The Catholic University of America, Washington, DC 20064, USA.ORCID 0000-0001-8647-9590
Gianna-Jade Del VecchioDepartment of Biology, The Catholic University of America, Washington, DC 20064, USA.ORCID 0000-0002-0791-402X
Joeffrey J ChahineDepartment of Biology, The Catholic University of America, Washington, DC 20064, USA.
Bhaskar V KallakuryDepartment of Pathology, MedStar Georgetown University Hospital, Washington, DC 20007, USA.
Pamela L TumaDepartment of Biology, The Catholic University of America, Washington, DC 20064, USA.
University of America · USGeorgetown University · US

Funding

Alcohol-induced changes in protein acetylation: mechanisms and consequencesR01AA017626 · NIAAA · CATHOLIC UNIVERSITY OF AMERICA · PI PAMELA L. TUMA · 2010 to 2026
$3.0M
NIAAA NIH HHS R01 AA017626NIH HHS AA017626NIH HHS DK082890
6 · The paper itself

Abstract

Recent studies report that the polarity gene myelin and lymphocyte protein 2 (MAL2), is overexpressed in multiple human carcinomas largely at the transcript level. Because chromosome 8q24 amplification (where MAL2 resides) is associated with hepatocellular- and cholangio-carcinomas, we examined MAL2 protein expression in these human carcinoma lesions and adjacent benign tissue using immunohistochemistry. For comparison, we analyzed renal cell carcinomas that are not associated with chromosome 8q24 amplification. Surprisingly, we found that MAL2 protein levels were decreased in the malignant tissues compared to benign in all three carcinomas, suggesting MAL2 expression may be anti-oncogenic. Consistent with this conclusion, we determined that endogenously overexpressed MAL2 in HCC-derived Hep3B cells or exogenously expressed MAL2 in hepatoma-derived Clone 9 cells (that lack endogenous MAL2) promoted actin-based protrusion formation with a reciprocal decrease in invadopodia. MAL2 overexpression also led to decreased cell migration, invasion and proliferation (to a more modest extent) while loss of MAL2 expression reversed the phenotypes. Mutational analysis revealed that a putative Ena/VASP homology 1 recognition site confers the MAL2-phenotype suggesting its role in tumor suppression involves actin remodeling. To reconcile decreased MAL2 protein expression in human carcinomas and its anti-oncogenic phenotypes with increased transcript levels, we propose a transcriptional regulatory model for MAL2 transient overexpression.

Indexed as

actincholangiocarcinomahepatocellular carcinomaMAL2tumor suppressor

Identifiers

PMID32059473
PMCPMC7072722
OpenAlexW3006299509

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.