ArticleMolecular and cellular biochemistry2014
The overexpression of MCPH1 inhibits cell growth through regulating cell cycle-related proteins and activating cytochrome c-caspase 3 signaling in cervical cancer.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Identification and validation of prognostic genes related to mitochondrial dynamics and mitochondrial autophagy in esophageal squamous cell carcinoma.Journal of thoracic disease · 2026Article
- TOP2A inhibition and its cellular effects related to cell cycle checkpoint adaptation pathway.Scientific reports · 2025Article
- The analyses of human MCPH1 DNA repair machinery and genetic variations.Open medicine (Warsaw, Poland) · 2024Article
- The emerging role of MCPH1/BRIT1 in carcinogenesis.Frontiers in oncology · 2023Review
- Multifaceted Microcephaly-Related Gene MCPH1.Cells · 2022Review
- Article
- The N-terminal BRCT domain determines MCPH1 function in brain development and fertility.Cell death & disease · 2021Article
- Analysis of the "centrosome-ome" identifies MCPH1 deletion as a cause of centrosome amplification in human cancer.Scientific reports · 2020Article
- The Yin and Yang of Autosomal Recessive Primary Microcephaly Genes: Insights from Neurogenesis and Carcinogenesis.International journal of molecular sciences · 2020Review
- Silencing BRIT1 Facilitates the Abilities of Invasiveness and Migration in Trophoblast Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Overexpression of MCPH1 inhibits the migration and invasion of lung cancer cells.OncoTargets and therapy · 2018Article
- The E3 ubiquitin ligase APC/CThe EMBO journal · 2017Article
- Overexpression of MCPH1 inhibits uncontrolled cell growth by promoting cell apoptosis and arresting the cell cycle in S and G2/M phase in lung cancer cells.Oncology letters · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MCPH1, initially identified as an hTERT repressor, has recently been implicated in mediating DNA damage response and maintaining chromosome integrity. This study is to investigate its potential role in the onset of cervical cancer. In the study, decreased expression of MCPH1 was observed in 19 of 31 cases (61.3%) at mRNA level and 44 of 63 cases (69.8%) at protein level of cervical tumor tissues compared with the paired nontumor tissues. Reduced MCPH1 protein expression was significantly associated with high-tumor grade (1 vs. 3 P = 0.013; 2 vs. 3 P = 0.047). In addition to inhibit SiHa cell migration and invasion, the overexpression of MCPH1 inhibited cervical cancer cells growth through inducing S phase arrest and mitochondrial apoptosis. Further analysis demonstrated cyclinA2/CDK2, CDC25C-cyclinB/CDC2, and p53/p21 pathways were involved in the MCPH1 overexpression-induced S phase arrest. Moreover, the overexpression of MCPH1 activated mitochondrial apoptosis through regulating several apoptosis-related proteins such as p53, Bcl-2, Bax, cytochrome c, caspase-3, and PARP-1. Our findings indicate that downregulated MCPH1 correlates with tumor progression in cervical cancer, and MCPH1 has an important role in regulating cell growth through regulating the cell cycle and apoptosis. Thus, it may be a crucial tumor suppressor gene and a novel candidate therapeutic target for cervical cancer.
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