ArticleMolecular and cellular biochemistry2014
P53 induction accompanying G2/M arrest upon knockdown of tumor suppressor HIC1 in U87MG glioma cells.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
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- The role and clinical relevance of long non-coding RNAs in glioma.Non-coding RNA research · 2023Article
- Hypermethylation of HIC2 is a potential prognostic biomarker and tumor suppressor of glioma based on bioinformatics analysis and experiments.CNS neuroscience & therapeutics · 2023Article
- PSMC2 knockdown suppressed tumor progression of skin cutaneous melanoma.Cell death discovery · 2021Article
- DNA methylation predicts age and provides insight into exceptional longevity of bats.Nature communications · 2021Article
- Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells.Cell reports · 2018Article
- Neurodevelopmental Genetic Diseases Associated With Microdeletions and Microduplications of Chromosome 17p13.3.Frontiers in genetics · 2018Review
- A critical overview of long non-coding RNA in glioma etiology 2016: an update.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- COL3A1 and SNAP91: novel glioblastoma markers with diagnostic and prognostic value.Oncotarget · 2016Article
- Dissecting dysfunctional crosstalk pathways regulated by miRNAs during glioma progression.Oncotarget · 2016Article
- Hypoxia inhibits mesenchymal stem cell proliferation through HIF1α-dependent regulation of P27.Molecular and cellular biochemistry · 2016Article
- Knockdown of PSF1 expression inhibits cell proliferation in lung cancer cells in vitro.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypermethylated in cancer 1 (HIC1) is a novel tumor suppressor gene (tsg) frequently silenced by epigenetic modification, predominantly by methylation in different tumors. HIC1 functionally co-operates with p53 in cultured cells as well as in transgenic animals to suppress tumors and has binding site on its promoter. Its over expression often leads to cell cycle arrests. Although HIC1 proven to have role as tsg, its regulation to cell cycle and dependency upon p53 is grossly unknown. In this study, we investigated the role of HIC1 in cell cycle and proliferation of glioma cell line U87MG which has wild type p53, in both serum-containing and serum-deprived medium. Microscopic analysis and MTT assay showed reduced cell number and rate of proliferation upon HIC1 knock down compared to control siRNA (p = 0.025) and untreated cells (p = 0.03) in serum-containing medium and serum-free medium (p = 0.014 vs control siRNA; p = 0.018 vs untreated cells). Cell cycle analysis revealed an arrest at G2/M phase of cell cycle with no demonstrable increase in apoptosis with both medium. An increased expression of p53 concomitant with HIC1 knockdown was observed. Furthermore P21, a p53 responsive gene, along with p27 was significantly increased in comparison with controls. Our results demonstrated an important role of HIC1 for the normal progression of cell cycle, and at molecular level, it could affect the homeostasis of p53 as well as number of cell cycle-related genes, which may or may not be directly linked to p53.
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