ArticleMolecular medicine (Cambridge, Mass.)2021
Inhibition of mitochondrial carrier homolog 2 (MTCH2) suppresses tumor invasion and enhances sensitivity to temozolomide in malignant glioma.
Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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.
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.
Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Neuronal differentiation regulator CEND1 coordinately suppresses tumor growth and energetics via AMPK signaling in brain glioma.Cell & bioscience · 2025Article
- MTCH2 Deficiency Promotes E2F4/TFRC-Mediated Ferroptosis and Sensitizes Colorectal Cancer Liver Metastasis to Sorafenib.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MTCH2 regulates NRF2-mediated RRM1 expression to promote melanoma proliferation and dacarbazine insensitivity.Cell death & disease · 2025Article
- Mitochondrial carrier homolog 2 is important for mitochondrial functionality and non-small cell lung cancer cell growth.Cell death & disease · 2025Article
- Identification of mitochondrial carrier homolog 2 as an important therapeutic target of castration-resistant prostate cancer.Cell death & disease · 2025Article
- The Role of Mitochondrial Solute Carriers SLC25 in Cancer Metabolic Reprogramming: Current Insights and Future Perspectives.International journal of molecular sciences · 2024Review
- MTCH2 promotes the malignant progression of ovarian cancer through the upregulation of AIMP2 expression levels, mitochondrial dysfunction and by mediating energy metabolism.Oncology letters · 2024Article
- MTCH2 stimulates cellular proliferation and cycles via PI3K/Akt pathway in breast cancer.Heliyon · 2024Article
- Mitochondrial carrier homolog 2 increases malignant phenotype of human gastric epithelial cells and promotes proliferation, invasion, and migration of gastric cancer cells.World journal of gastrointestinal oncology · 2024Article
- Preparation of transferrin-targeted temozolomide nano-micelles and their anti-glioma effect.PeerJ · 2024Article
- MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction.Drug design, development and therapy · 2024Review
- Clinical and molecular analysis of cilia-associated gene signature for prognostic prediction in glioma.Journal of cancer research and clinical oncology · 2023Article
- APOC1 promotes the progression of osteosarcoma by binding to MTCH2.Experimental and therapeutic medicine · 2023Article
- Identification of Genetic Alterations in Rapid Progressive Glioblastoma by Use of Whole Exome Sequencing.Diagnostics (Basel, Switzerland) · 2023Article
- Integrative analysis defines DDIT3 amplification as a correlative and essential factor for glioma malignancy.American journal of cancer research · 2023Article
- The platinum coordination complex inhibits cell invasion-migration and epithelial-to-mesenchymal transition by altering the TGF-β-SMAD pathway in colorectal cancer.Frontiers in pharmacology · 2023Article
- Analysis of somatic mutations and key driving factors of cervical cancer progression.Open medicine (Warsaw, Poland) · 2023Article
- Mitochondrial dynamics involves molecular and mechanical events in motility, fusion and fission.Frontiers in cell and developmental biology · 2022Review
- Small Interfering RNA for Gliomas Treatment: Overcoming Hurdles in Delivery.Frontiers in cell and developmental biology · 2022Review
- Expanding the Genetic Blueprint of Wilms Tumor: An Account of 71 Novel Variants across 16 Genes with Novel Implications for Wilms Tumor Pathogenesis.Journal of Indian Association of Pediatric SurgeonsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMalignant glioma exerts a metabolic shift from oxidative phosphorylation (OXPHOs) to aerobic glycolysis, with suppressed mitochondrial functions. This phenomenon offers a proliferation advantage to tumor cells and decrease mitochondria-dependent cell death. However, the underlying mechanism for mitochondrial dysfunction in glioma is not well elucidated. MTCH2 is a mitochondrial outer membrane protein that regulates mitochondrial metabolism and related cell death. This study aims to clarify the role of MTCH2 in glioma.
methodsBioinformatic analysis from TCGA and CGGA databases were used to investigate the association of MTCH2 with glioma malignancy and clinical significance. The expression of MTCH2 was verified from clinical specimens using real-time PCR and western blots in our cohorts. siRNA-mediated MTCH2 knockdown were used to assess the biological functions of MTCH2 in glioma progression, including cell invasion and temozolomide-induced cell death. Biochemical investigations of mitochondrial and cellular signaling alternations were performed to detect the mechanism by which MTCH2 regulates glioma malignancy.
resultsBioinformatic data from public database and our cohort showed that MTCH2 expression was closely associated with glioma malignancy and poor patient survival. Silencing of MTCH2 expression impaired cell migration/invasion and enhanced temozolomide sensitivity of human glioma cells. Mechanistically, MTCH2 knockdown may increase mitochondrial OXPHOs and thus oxidative damage, decreased migration/invasion pathways, and repressed pro-survival AKT signaling.
conclusionOur work establishes the relationship between MTCH2 expression and glioma malignancy, and provides a potential target for future interventions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.