Evidence map›Paper›PMID 32801758›Full record

ArticleOncoTargets and therapy2020

Methylcrotonoyl-CoA Carboxylase 2 Promotes Proliferation, Migration and Invasion and Inhibits Apoptosis of Prostate Cancer Cells Through Regulating GLUD1-P38 MAPK Signaling Pathway.

Jianwen He, Yunhua Mao, Wentao Huang, Mingzhao Li, Huimin Zhang, Yunhao Qing, Shuo Lu, Hengjun Xiao, Ke Li

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  7. Cellular Signaling of Amino Acid Metabolism in Prostate Cancer.International journal of molecular sciences · 2025
    Review
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  13. Review
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  18. The Effect of Avidin on Viability and Proliferation of Colorectal Cancer Cells HT-29.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  19. Article
  20. Article
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

9 authors at 1 institution in 1 country.

Jianwen He *Department of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.ORCID 0000-0002-8390-0834
Yunhua Mao *Department of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.
Wentao Huang *Department of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.
Mingzhao LiDepartment of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.
Huimin ZhangDepartment of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.
Yunhao QingDepartment of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.
Shuo LuDepartment of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.
Hengjun XiaoDepartment of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.ORCID 0000-0001-5472-2154
Ke LiDepartment of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, People's Republic of China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeProstate cancer (PCa) is the most common cancer in American men, and the mechanisms of development and progression are still not completely clear. Methylcrotonoyl-CoA carboxylase 2 (MCCC2) was previously identified overexpressed in PCa with lymph node metastasis, but its specific role and mechanisms need further investigation. This study aimed to investigate the role of MCCC2 in PCa cells and its underlying mechanisms. MATERIALS AND

methodsQuantitative RT-PCR and Western blotting were used to detect MCCC2 mRNA and protein expression in normal prostate epithelium and cancerous cells. Upon manipulation of MCCC2 expression, cell proliferation was measured by CCK-8 assays and migration and invasion were determined by transwell assays. Changes of apoptosis, cell cycle and mitochondrial membrane potential were evaluated by flow cytometry. MCCC2-mediated signaling pathways were screened by bioinformatics and verified by RT-PCR and Western blotting. Finally, immunohistochemistry was performed to detect the expression of MCCC2 and glutamate dehydrogenase 1 (GLUD1) in PCa tissues to analyze their correlation.

resultsWe demonstrated that MCCC2 promoted cell proliferation, migration and invasion but inhibited apoptosis in PCa cells. In addition, MCCC2 in 22Rv1 cells induced mitochondrial damage. In PCa tissues, MCCC2 overexpression associated with lymph node metastasis (

conclusionMCCC2 exerts oncogenic function in PCa through regulating GLUD1-p38 MAPK signaling pathway, and it may be a potential treatment target.

Indexed as

GLUD1MCCC2p38 MAPKprostate cancer

Identifiers

PMID32801758
PMCPMC7395692
OpenAlexW3044961690

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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.