Evidence map›Paper›PMID 36911382›Full record

ArticleExperimental and therapeutic medicine2023

APOC1 promotes the progression of osteosarcoma by binding to MTCH2.

Renjie Li, Huixian He, Xinxin He

Abstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

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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

3 authors.

Renjie LiSchool of Nursing, Sun Yat-Sen University, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Huixian HeDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Xinxin HeSchool of Medicine, Foshan University, Foshan, Guangdong 528000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma is the most prevalent primary malignant bone cancer worldwide. Apolipoprotein C1 (APOC1) and mitochondrial carrier homolog 2 (MTCH2) have been identified to be upregulated during the oncogenesis and metastasis of osteosarcoma. The aim of the present study was to explore the role of APOC1 in osteosarcoma progression and the mechanisms associated with MTCH2. APOC1 and MTCH2 expression in osteosarcoma cells was assessed by reverse transcription-quantitative PCR and western blotting. Then, APOC1 was silenced to detect its effect on cell viability, proliferation and apoptosis using Cell Counting Kit-8, a colony formation assay and TUNEL staining, respectively. Transwell and wound healing assays were used to evaluate cell invasion and migration. The interaction between APOC1 and MTCH2 as predicted by the Biological General Repository for Interaction Datasets and the Search Tool for the Retrieval of Interacting Genes/Proteins databases was verified by co-immunoprecipitation assay. Subsequently, rescue experiments were performed to analyze the regulatory effects of APOC1 on MTCH2 in the biological behavior and Warburg effect of osteosarcoma cells. Significantly upregulated APOC1 and MTCH2 expression was found in osteosarcoma SAOS-2 cells. APOC1 silencing attenuated cell viability, inhibited proliferation and promoted cell apoptosis, coupled with the decreased Bcl-2 expression and increased Bax and cleaved-caspase 3 expression. The invasive and migratory capacities of SAOS-2 cells were also suppressed following APOC1 knockdown. Moreover, APOC1 was confirmed to interact with MTCH2 in osteosarcoma cells. MTCH2 upregulation inhibited the impacts of APOC1 deletion on the malignant behavior of osteosarcoma cells. APOC1 silencing-induced oxidative phosphorylation elevation and Warburg effect decrease were partially restored by MTCH2 upregulation. In sum, APOC1 promoted progression of osteosarcoma by binding to MTCH2, suggesting that targeting the APOC1/MTCH2 axis may be a potential treatment of osteosarcoma.

Indexed as

apolipoprotein C1invasionmitochondrial carrier homolog 2osteosarcomaWarburg effect

Identifiers

PMID36911382
PMCPMC9996334

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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.