Evidence map›Paper›PMID 38064181›Full record

ArticleCancer reports (Hoboken, N.J.)2023

MMP-2 regulates Src activation via repression of the CHK/MATK tumor suppressor in osteosarcoma.

Deanna V Maybee, Christopher R Cromwell, Basil P Hubbard, Mohammad A M Ali

Open access · goldAbstract read
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 7 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

4 authors at 2 institutions in 2 countries.

Deanna V MaybeeDepartment of Pharmaceutical Sciences, SUNY Binghamton University School of Pharmacy and Pharmaceutical Sciences, Binghamton, New York, USA.
Christopher R CromwellDepartment of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.
Basil P HubbardDepartment of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.
Mohammad A M AliDepartment of Pharmaceutical Sciences, SUNY Binghamton University School of Pharmacy and Pharmaceutical Sciences, Binghamton, New York, USA.ORCID https://orcid.org/0000-0002-6404-4198
Binghamton University · USUniversity of Toronto · CA

Funding

Research Foundation for the State University of New York 910252-50
6 · The paper itself

Abstract

backgroundDoxorubicin, a first-line anticancer drug for osteosarcoma treatment, has been the subject of recent research exploring the mechanisms behind its chemoresistance and its ability to enhance cell migration at sublethal concentrations. Matrix metalloproteinase-2 (MMP-2), a type IV collagenase and zinc-dependent endopeptidase, is well-known for degrading the extracellular matrix and promoting cancer metastasis. Our previous work demonstrated that nuclear MMP-2 regulates ribosomal RNA transcription via histone clipping, thereby controlling gene expression. Additionally, MMP-2 activity is regulated by the non-receptor tyrosine kinase and oncogene, Src, which plays a crucial role in cell adhesion, invasion, and metastasis. Src kinase is primarily regulated by two endogenous inhibitors: C-terminal Src kinase (Csk) and Csk homologous kinase (CHK/MATK).

aimIn this study, we reveal that the MMP-2 gene acts as an upstream regulator of Src kinase activity by suppressing its endogenous inhibitor, CHK/MATK, in osteosarcoma cells. METHODS AND

resultsWe show that enhanced osteosarcoma cell migration which is induced by sublethal concentrations of doxorubicin can be overcome by inactivating the MMP-2 gene or overexpressing CHK/MATK. Our findings highlight the MMP-2 gene as a promising additional target for combating cancer cell migration and metastasis. This is due to its role in suppressing on the gene and protein expression of the tumor suppressor CHK/MATK in osteosarcoma.

conclusionBy targeting the MMP-2 gene, we can potentially enhance the effectiveness of doxorubicin treatment and reduce chemoresistance in osteosarcoma.

Indexed as

Csk homologous kinase (CHK/MATK)doxorubicinmatrix metalloproteinase-2 (MMP-2)osteosarcomaSrcSrc family kinases (SFK)

Identifiers

PMID38064181
PMCPMC10849928
OpenAlexW4389476558

What OpenQuestion holds

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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.