Evidence map›Paper›PMID 33407468›Full record

ArticleCancer cell international2021

MCCC2 promotes HCC development by supporting leucine oncogenic function.

Yu-Yan Chen, Xue-Ning Zhang, Chen-Zhou Xu, Dan-Hua Zhou, Jing Chen, Zhao-Xiu Liu, Ying Sun, Wei Huang, Li-Shuai Qu

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 36 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

9 authors at 3 institutions in 1 country.

Yu-Yan ChenDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong, China.ORCID http://orcid.org/0000-0002-8489-6961
Xue-Ning ZhangDepartment of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, China.
Chen-Zhou XuDepartment of Gastroenterology, The First Hospital of Jiaxing, Affiliated Hospital of Jiaxing University, Jiaxing, China.
Dan-Hua ZhouDepartment of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, China.
Jing ChenResearch Center of Clinical Medicine, Nantong University, Affiliated Hospital of Nantong University, Nantong, China.
Zhao-Xiu LiuDepartment of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, China.
Ying SunBlood Center of Jiangsu Province, Nanjing, China.
Wei HuangDepartment of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, China. huangweint@ntu.edu.cn.
Li-Shuai QuDepartment of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, China. qulishuai1121@163.com.
Nantong University · CNJiangsu Province Blood Center · CNJiaxing University · CN

Funding

Key Research and Development Plan of Jiangsu Province No.BE2019692Postdoctoral Foundation of Hei Long Jiang Province (CN) Grant No.2019M661909Social Development Foundation of Nantong City Grant.nos.JC2019032; MS12019020Young Medical Talent Project of Jiangsu Province QNRC2016697
6 · The paper itself

Abstract

backgroundThe role of methylcrotonoyl-CoA carboxylase 2 (MCCC2) in the development of tumors is well-established, and the involvement of leucine in the liver is well-known. However, the role of MCCC2 and the correlation between MCCC2 and leucine in the progression of hepatocellular carcinoma (HCC) have not yet been reported.

methodsIn this study, the Gepia database was used to evaluate the prognostic value of MCCC2 in HCC. The expression and localization of MCCC2 in HCC cells were determined by western blot and immunofluorescence assays. Flow cytometry and CCK-8 and transwell assays were carried out to explore the effect of MCCC2 on cell proliferation, migration, and invasion. In addition, mass spectrometry analysis was used to predict the potential cell function of MCCC2 in HCC.

resultsWe found that the expression of MCCC2 increased in HCC tissues and that high expression of MCCC2 could predict poor outcomes in HCC patients. Knockdown expression of MCCC2 in HCC cells could reduce cell proliferation, migration, and invasion ability in vitro and could inhibit HCC cell proliferation in vivo. Interestingly, we found that HCC cells transfected with MCCC2-sgRNA failed to respond to leucine deprivation. Meanwhile, leucine deprivation inhibited cell proliferation, migration, and invasion in HCC cells where MCCC2 was present rather than in cells where MCCC2 was absent. In addition, knockdown of MCCC2 significantly reduced the glycolysis markers, glucose consumption, lactate secretion, and acetyl-CoA level, which is a product of leucine metabolism. Furthermore, we found that MCCC2 promotes the activation of ERK. Profiling the MCCC2 binding proteins revealed that MCCC2-associated proteins are enriched in biological processes, such as protein metabolism, energy pathway, and metabolism in HCC cells.

conclusionsOur findings revealed that MCCC2 plays a critical role in the development of HCC, and the leucine metabolism pathway might be a novel target in HCC treatment.

Indexed as

ERKHepatocellular carcinomaleucineMCCC2metabolism

Identifiers

PMID33407468
PMCPMC7788835
OpenAlexW3121079320

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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.