ArticleInternational journal of clinical and experimental pathology2015
Kank1 reexpression induced by 5-Aza-2'-deoxycytidine suppresses nasopharyngeal carcinoma cell proliferation and promotes apoptosis.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- TSLP enhances progestin response in endometrial cancer via androgen receptor signal pathway.British journal of cancer · 2024Article
- An Emerging Role for Epigenetics in Cerebral Palsy.Journal of personalized medicine · 2021Review
- Article
- Derivative of Stevioside; CPUK02; Restores ESR1 Gene Methylation in MDA-MB 231Asian Pacific journal of cancer prevention : APJCP · 2018Article
- Combined Treatment with Valproic Acid and 5-Aza-2'-Deoxycytidine Synergistically Inhibits Human Clear Cell Renal Cell Carcinoma Growth and Migration.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- miR-375 is downregulated by promoter hypermethylation in MIN6 insulinoma cells.International journal of clinical and experimental pathology · 2018Article
- KANK1 inhibits cell growth by inducing apoptosis through regulating CXXC5 in human malignant peripheral nerve sheath tumors.Scientific reports · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kank1, which was first described as a potential tumor suppressor for renal cell carcinoma (RCC), mapped to 9p24.3 and encoded an ankyrin-repeat domain-containing protein. Its frequent deletion was found to be associated with several human malignant tumors, cerebral palsy, and neuronal and developmental diseases. However, its functional role in nasopharyngeal cancer (NPC) was still unknown. In the present study, we found that Kank1 expression was down-regulated in NPC cells than in human nasopharyngeal epithelial cell line NP69 and demethylating agent 5-aza-2'-deoxycytidine (5-aza-CdR) could improve its mRNA and protein expression level. Further studies demonstrated that DNA methylation might be the mainly cause for Kank1 decreased expression and restored Kank1 expression mediated by 5-aza-CdR played a key role in suppressing NPC cells growth and inducing its apoptosis. Our primary results revealed new function of Kank1 for NPC and implied that epigenetic regulation especially demethylation may have a potential value for NPC treatment.
Indexed as
Identifiers
25973051PMC4396205W2464943538What 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.