ArticleCancer research2011
S6 kinase 2 promotes breast cancer cell survival via Akt.
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 32 papers.
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Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- USF1-induced RPS6KB2 activation influences aggressive phenotype in B-cell non-Hodgkin lymphoma.Human cell · 2025Article
- The splicing factor SRRM2 modulates two S6K kinases to promote colorectal cancer growth.Oncogene · 2025Article
- Selective abrogation of S6K2 identifies lipid homeostasis as a survival vulnerability in MAPK inhibitor-resistantScience translational medicine · 2025Article
- S6K2 in Focus: Signaling Pathways, Post-Translational Modifications, and Computational Analysis.International journal of molecular sciences · 2024Review
- p21Cancers · 2024Article
- ALYREF recruits ELAVL1 to promote colorectal tumorigenesis via facilitating RNA m5C recognition and nuclear export.NPJ precision oncology · 2024Article
- Coordinated Targeting of S6K1/2 and AXL Disrupts Pyrimidine Biosynthesis in PTEN-Deficient Glioblastoma.Cancer research communications · 2024Article
- Rapamycin increases leukemia cell sensitivity to chemotherapy by regulating mTORC1 pathway-mediated apoptosis and autophagy.International journal of hematology · 2024Article
- Ribosomal protein S6 kinase 2 (RPS6KB2) is a potential immunotherapeutic target for cancer that upregulates proinflammatory cytokines.Molecular biology reports · 2024Article
- The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products.Antioxidants (Basel, Switzerland) · 2022Review
- Cordycepin augments the chemosensitivity of osteosarcoma to cisplatin by activating AMPK and suppressing the AKT signaling pathway.Cancer cell international · 2021Article
- Pharmacologic inhibition of Akt in combination with chemotherapeutic agents effectively induces apoptosis in ovarian and endometrial cancer cell lines.Molecular oncology · 2021Article
- Article
- Distinct Roles of mTOR Targets S6K1 and S6K2 in Breast Cancer.International journal of molecular sciences · 2020Review
- TRAIL-induced variation of cell signaling states provides nonheritable resistance to apoptosis.Life science alliance · 2019Article
- Relationship between Ribosomal Protein S6-pS240 Expression and other Prognostic Factors in Non-Special Type Invasive Breast Cancer.Breast care (Basel, Switzerland) · 2019Article
- CLK2 blockade modulates alternative splicing compromising MYC-driven breast tumors.EMBO molecular medicine · 2018Article
- p53 and metabolism: from mechanism to therapeutics.Oncotarget · 2018Review
- Mammalian EAK-7 activates alternative mTOR signaling to regulate cell proliferation and migration.Science advances · 2018Article
- Gene Expression Patterns Analysis in the Supraspinatus Muscle after a Rotator Cuff Tear in a Mouse Model.BioMed research international · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The 40S ribosomal protein S6 kinase (S6K) acts downstream of mTOR, which plays important roles in cell proliferation, protein translation, and cell survival and is a target for cancer therapy. mTOR inhibitors are, however, of limited success. Although Akt is believed to act upstream of mTOR, persistent inhibition of p70 S6 kinase or S6K1 can activate Akt via a negative feedback loop. S6K exists as two homologues, S6K1 and S6K2, but little is known about the function of S6K2. In the present study, we have examined the effects of S6K2 on Akt activation and cell survival. Silencing of S6K1 caused a modest decrease, whereas knockdown of S6K2 caused a substantial increase in TNF-α and TRAIL (TNF-related apoptosis-inducing ligand)-mediated apoptosis. In contrast to S6K1, depletion of S6K2 by siRNA decreased basal and TNF-induced Akt phosphorylation. Ectopic expression of constitutively active Akt in MCF-7 cells restored cell survival in S6K2-depleted cells. We have previously shown that activation of Akt induces downregulation of Bid via p53. Knockdown of S6K2 caused an increase in p53, and downregulation of p53 by siRNA decreased Bid level. Silencing of Bid blunted the ability of S6K2 deficiency to enhance TNF-induced apoptosis. Taken together, our study shows that the two homologues of S6K have distinct effects on Akt activation and cell survival. Thus, targeting S6K2 may be an effective therapeutic strategy to treat cancers.
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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.