Open Access

MTCH2 promotes the malignant progression of ovarian cancer through the upregulation of AIMP2 expression levels, mitochondrial dysfunction and by mediating energy metabolism 

  • Authors:
    • Guangyu Sun
    • Yanmin Song
    • Congxian Li
    • Bo Sun
    • Chengcheng Li
    • Jinbao Sun
    • Ping Xiao
    • Zhengmao Zhang
  • View Affiliations

  • Published online on: August 12, 2024     https://doi.org/10.3892/ol.2024.14625
  • Article Number: 492
  • Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ovarian cancer (OC) is a gynecological malignancy that ranks among the most common female cancers worldwide and notably reduces a patient's quality of life. Mitochondrial carrier homology 2 (MTCH2) is a mitochondrial outer membrane protein that serves a regulatory role in mitochondrial metabolism and cell death. The precise contribution and underlying molecular pathways of MTCH2 in the context of OC development is currently unclear. The present study aimed to investigate the roles of MTCH2 in the energy metabolism, cell proliferation and metastatic potential of OC cells and evaluate the regulatory relationship between MTCH2, aminoacyl transfer RNA synthetase‑interacting multifunctional protein 2 (AIMP2) and claudin‑3. An analysis of 67 patients with high‑grade serous OC demonstrated increased expression levels of MTCH2, AIMP2 and claudin‑3 in OC tumor tissue samples compared with in corresponding normal tissues adjacent to OC tissue samples. MTCH2 overexpression was significantly associated with the International Federation of Gynecology and Obstetrics stage and tumor differentiation of the OC tumor samples. In vitro experiments using the SK‑OV‑3 OC cell line demonstrated that MTCH2 exerts a regulatory effect on the cell proliferation, invasion and migratory capabilities of these cells. Knockdown of MTCH2 reduced ATP production, induced mitochondrial dysfunction and promoted cytoskeleton remodeling and apoptosis in SK‑OV‑3 OC cells. In addition, MTCH2 knockdown downregulated the expression levels of both claudin‑3 and AIMP2 proteins. Knockdown of AIMP2 inhibited the regulatory effect of MTCH2. Co‑immunoprecipitation experiments demonstrated that MTCH2 interacts with AIMP2 and claudin‑3. The present study provides novel insights into the treatment of OC metastasis, as MTCH2 was demonstrated to serve roles in the progression of OC cells through the regulation of claudin‑3 via AIMP2, which could provide novel insights into the treatment of ovarian cancer metastasis.
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October-2024
Volume 28 Issue 4

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Online ISSN:1792-1082

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Copy and paste a formatted citation
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Spandidos Publications style
Sun G, Song Y, Li C, Sun B, Li C, Sun J, Xiao P and Zhang Z: MTCH2 promotes the malignant progression of ovarian cancer through the upregulation of AIMP2 expression levels, mitochondrial dysfunction and by mediating energy metabolism . Oncol Lett 28: 492, 2024.
APA
Sun, G., Song, Y., Li, C., Sun, B., Li, C., Sun, J. ... Zhang, Z. (2024). MTCH2 promotes the malignant progression of ovarian cancer through the upregulation of AIMP2 expression levels, mitochondrial dysfunction and by mediating energy metabolism . Oncology Letters, 28, 492. https://doi.org/10.3892/ol.2024.14625
MLA
Sun, G., Song, Y., Li, C., Sun, B., Li, C., Sun, J., Xiao, P., Zhang, Z."MTCH2 promotes the malignant progression of ovarian cancer through the upregulation of AIMP2 expression levels, mitochondrial dysfunction and by mediating energy metabolism ". Oncology Letters 28.4 (2024): 492.
Chicago
Sun, G., Song, Y., Li, C., Sun, B., Li, C., Sun, J., Xiao, P., Zhang, Z."MTCH2 promotes the malignant progression of ovarian cancer through the upregulation of AIMP2 expression levels, mitochondrial dysfunction and by mediating energy metabolism ". Oncology Letters 28, no. 4 (2024): 492. https://doi.org/10.3892/ol.2024.14625