ArticleOncogene2004
The tumor suppressor p16(INK4a) gene is a regulator of apoptosis induced by ultraviolet light and cisplatin.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 67 citations in OpenAlex.
- Article
- Immunohistochemical Study of Airways Fibrous Remodeling in Smoking Mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- Cellular senescence induction leads to progressive cell death via the INK4a-RB pathway in naked mole-rats.The EMBO journal · 2023Article
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
- Cellular Senescence: Mechanisms and Therapeutic Potential.Biomedicines · 2021Review
- Deletion of Nrip1 delays skin aging by reducing adipose-derived mesenchymal stem cells (ADMSCs) senescence, and maintaining ADMSCs quiescence.GeroScience · 2021Article
- Role of Long Non-Coding RNA Polymorphisms in Cancer Chemotherapeutic Response.Journal of personalized medicine · 2021Review
- Review
- Expression and role of p16 and GLUT1 in malignant diseases and lung cancer: A review.Thoracic cancer · 2020Review
- Boolean model of growth signaling, cell cycle and apoptosis predicts the molecular mechanism of aberrant cell cycle progression driven by hyperactive PI3K.PLoS computational biology · 2019Article
- The deficiency of CX3CL1/CX3CR1 system ameliorates high fructose diet-induced kidney injury by regulating NF-κB pathways in CX3CR1-knock out mice.International journal of molecular medicine · 2018Article
- Inhibition of coiled coil domain containing protein 69 enhances platinum-induced apoptosis in ovarian cancer cells.Oncotarget · 2017Article
- p16Molecular carcinogenesis · 2017Article
- C-terminal binding protein-2 promotes cell proliferation and migration in breast cancer via suppression of p16INK4A.Oncotarget · 2017Article
- Association between well-characterized lung cancer lncRNA polymorphisms and platinum-based chemotherapy toxicity in Chinese patients with lung cancer.Acta pharmacologica Sinica · 2017Article
- Disruption of PCNA-lamins A/C interactions by prelamin A induces DNA replication fork stalling.Nucleus (Austin, Tex.) · 2016Article
- Association of well-characterized lung cancer lncRNA polymorphisms with lung cancer susceptibility and platinum-based chemotherapy response.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- p16 Protein and gigaxonin are associated with the ubiquitination of NFκB in cisplatin-induced senescence of cancer cells.The Journal of biological chemistry · 2014Article
- The cyclin-dependent kinase inhibitor p16INK4a physically interacts with transcription factor Sp1 and cyclin-dependent kinase 4 to transactivate microRNA-141 and microRNA-146b-5p spontaneously and in response to ultraviolet light-induced DNA damage.The Journal of biological chemistry · 2013Article
- INK4a/ARF limits the expansion of cells suffering from replication stress.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p16(INK4a) (hereafter referred to as p16), a major cyclin-dependent kinase (CDK) inhibitor, is the product of a tumor-suppressor gene that has been found inactivated in different cancer types. In the present study, we sought to investigate the role of p16 in apoptosis induced by ultraviolet light (the most important etiological cause of skin cancer) and cisplatin (an anticancer DNA damaging agent). It is clearly shown that p16-compromised osteosarcoma U2OS cell line and p16-/- mouse embryo fibroblasts are sensitive to UV-induced apoptosis, as compared to their respective isogenic p16-expressing cells (EH1, EH2) and p16 +/+, indicating that p16 protects cells from undergoing apoptosis in response to UV light. Importantly, this reduction in UV-mediated apoptosis was associated with downregulation of the proapoptotic Bax protein, with no effect on Bcl-2 expression, suggesting that this antiapoptotic role of p16 is mediated via the intrinsic-mitochondrial pathway. On the other hand, p16 sensitized cells to cisplatin-mediated apoptosis through Bcl-2 decline. Interestingly, only proliferating but not G1-arrested EH1 cells underwent apoptosis in response to the anticancer drug. These novel findings provide further insight into the role of p16 in carcinogenesis, and has potential implications for future therapy strategies.
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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.