ArticleProceedings of the National Academy of Sciences of the United States of America2010
Kinase requirements in human cells: V. Synthetic lethal interactions between p53 and the protein kinases SGK2 and PAK3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. 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, 90 citations in OpenAlex.
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- Differentially expressed genes associated with high metabolic tumor volume served as diagnostic markers and potential therapeutic targets for pancreatic cancer.Journal of translational medicine · 2024Article
- The molecular mechanism and challenge of targeting XPO1 in treatment of relapsed and refractory myeloma.Translational oncology · 2022Review
- Two differentially methylated region networks in nonalcoholic fatty liver disease, viral hepatitis, and hepatocellular carcinoma.BMC gastroenterology · 2022Article
- ATM Pathway Is Essential for HPV-Positive Human Cervical Cancer-Derived Cell Lines Viability and Proliferation.Pathogens (Basel, Switzerland) · 2022Article
- SGK2, 14-3-3, and HUWE1 Cooperate to Control the Localization, Stability, and Function of the Oncoprotein PTOV1.Molecular cancer research : MCR · 2022Article
- Label-free affinity screening, design and synthesis of inhibitors targeting the Mycobacterium tuberculosis L-alanine dehydrogenase.PloS one · 2022Article
- Interplay between HMGA and TP53 in cell cycle control along tumor progression.Cellular and molecular life sciences : CMLS · 2021Review
- Advances in synthetic lethality for cancer therapy: cellular mechanism and clinical translation.Journal of hematology & oncology · 2020Review
- Prognosis, Biology, and Targeting ofCells · 2020Review
- Review
- Identification of TP53RK-Binding Protein (TPRKB) Dependency inMolecular cancer research : MCR · 2019Article
- Inhibition of Thioredoxin/Thioredoxin Reductase Induces Synthetic Lethality in Lung Cancers with Compromised Glutathione Homeostasis.Cancer research · 2019Article
- Regulation of Apoptosis During Porcine Circovirus Type 2 Infection.Frontiers in microbiology · 2018Review
- Molecularly targeted therapies for p53-mutant cancers.Cellular and molecular life sciences : CMLS · 2017Review
- The kinome 'at large' in cancer.Nature reviews. Cancer · 2016Review
- Molecular Aspects of Head and Neck Cancer Therapy.Hematology/oncology clinics of North America · 2015Review
- Transcriptomic analysis of pancreatic cancer cells in response to metformin and aspirin: an implication of synergy.Scientific reports · 2015Article
- Lethality of PAK3 and SGK2 shRNAs to human papillomavirus positive cervical cancer cells is independent of PAK3 and SGK2 knockdown.PloS one · 2015Article
- MicroRNA 9-3p targets β1 integrin to sensitize claudin-low breast cancer cells to MEK inhibition.Molecular and cellular biology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Cervical carcinomas are initiated through a series of well-defined stages that rely on the expression of human papillomavirus (HPV) oncogenes. A panel of 100 small hairpin RNAs that target essential kinases in many tumor types was used to study the stepwise appearance of kinase requirements during cervical tumor development. Twenty-six kinases were commonly required in three cell lines derived from frank carcinomas, and each kinase requirement was traced to the specific stage in which the requirement emerged. Six kinases became required following HPV-induced immortalization, and the requirement for two kinases, SGK2 and PAK3, was mapped to the inactivation of p53 in primary human epithelial cells. Loss of the p53 tumor suppressor in other primary epithelial cells also induced dependence on SGK2 and PAK3. Hence, SGK2 and PAK3 provide important cellular functions following p53 inactivation, fulfilling the classical definition of synthetic lethality; loss of p53, SGK2, or PAK3 alone has little effect on cell viability, whereas loss of p53 together with either SGK2 or PAK3 loss leads to cell death. Whereas tumor suppressor gene mutations are not directly druggable, other proteins or pathways that become obligatory to cell viability following tumor suppressor loss provide theoretical targets for tumor suppressor-specific drug discovery efforts. The kinases SGK2 and PAK3 may thus represent such targets for p53-specific drug development.
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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.