ArticleCancer research2011
DeltaNp63alpha confers tumor cell resistance to cisplatin through the AKT1 transcriptional regulation.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Role of DNA methylation and non‑coding RNAs expression in pathogenesis, detection, prognosis, and therapy‑resistant ovarian carcinoma (Review).Molecular medicine reports · 2025Review
- TIP60 enhances cisplatin resistance via regulating ΔNp63α acetylation in SCC.Cell death & disease · 2024Article
- The mitochondrial inhibitor IF1 binds to the ATP synthase OSCP subunit and protects cancer cells from apoptosis.Cell death & disease · 2023Article
- Inhibition of SRPK1, a key splicing regulator, exhibits antitumor and chemotherapeutic-sensitizing effects on extranodal NK/T-cell lymphoma cells.BMC cancer · 2022Article
- Signaling pathways and targeted therapies in lung squamous cell carcinoma: mechanisms and clinical trials.Signal transduction and targeted therapy · 2022Review
- A comprehensive survey into the role of microRNAs in ovarian cancer chemoresistance; an updated overview.Journal of ovarian research · 2022Review
- Inhibition of USP28 overcomes Cisplatin-resistance of squamous tumors by suppression of the Fanconi anemia pathway.Cell death and differentiation · 2022Article
- LINC00324 in cancer: Regulatory and therapeutic implications.Frontiers in oncology · 2022Review
- ΔN63 suppresses the ability of pregnancy-identified mammary epithelial cells (PIMECs) to drive HER2-positive breast cancer.Cell death & disease · 2021Article
- Targeting of ΔNp63α by miR-522 promotes the migration of breast epithelial cells.FEBS open bio · 2021Article
- The Non-Coding RNAs Inducing Drug Resistance in Ovarian Cancer: A New Perspective for Understanding Drug Resistance.Frontiers in oncology · 2021Review
- Disruption of TP63-miR-27a* Feedback Loop by Mutant TP53 in Head and Neck Cancer.Journal of the National Cancer Institute · 2020Article
- Article
- Activating p53 family member TAp63: A novel therapeutic strategy for targeting p53-altered tumors.Cancer · 2019Article
- IL-1β Inflammatory Cytokine-InducedInternational journal of molecular sciences · 2019Article
- A double dealing tale of p63: an oncogene or a tumor suppressor.Cellular and molecular life sciences : CMLS · 2018Review
- Therapeutic implications of cellular and molecular biology of cancer stem cells in melanoma.Molecular cancer · 2017Review
- Autologous reconstitution of human cancer and immune system in vivo.Oncotarget · 2017Article
- ΔNp63 activates the Fanconi anemia DNA repair pathway and limits the efficacy of cisplatin treatment in squamous cell carcinoma.Nucleic acids research · 2016Article
- 1α, 25-Dihydroxyvitamin D₃ and the vitamin D receptor regulates ΔNp63α levels and keratinocyte proliferation.Cell death & disease · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Strategies to address resistance to platin drugs are greatly needed in human epithelial cancers (e.g., ovarian, head/neck, and lung) where platins are used widely and resistance occurs commonly. We found that upon ΔNp63α overexpression, AKT1 and phospho-AKT1 levels are upregulated in cancer cells. Investigations using gel-shift, chromatin immunoprecipitation and functional reporter assays implicated ΔNp63α in positive regulation of AKT1 transcription. Importantly, we found that ΔNp63α, AKT1, and phospho-AKT levels are greater in 2008CI3 CDDP-resistant ovarian cancer cells than in 2008 CDDP-sensitive cells. siRNA-mediated knockdown of ΔNp63α expression dramatically decreased AKT1 expression, whereas knockdown of either ΔNp63α or AKT1 decreased cell proliferation and increased death of ovarian and head/neck cancer cells. Conversely, enforced expression of ΔNp63α increased cancer cell proliferation and reduced apoptosis. Together, our findings define a novel ΔNp63α-dependent regulatory mechanism for AKT1 expression and its role in chemotherapeutic resistance of ovarian and head/neck cancer cells.
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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.