ArticleInternational journal of molecular sciences2024
S6K1 Controls DNA Damage Signaling Modulated by the MRN Complex to Induce Radioresistance in Lung Cancer.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- S6K1 Modulates STAT3 Activation to Promote Resistance to Radiotherapy in Lung Cancer.International journal of molecular sciences · 2026Article
- MmuPV1 E7 promotes phenotypes associated with "high-risk" HPV infection in mouse keratinocytes.Journal of virology · 2025Article
- Evaluating the efficacy of PARP inhibitor in ARID1A-deficient colorectal cancer: ACancer biomarkers : section A of Disease markers · 2025Article
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3 authors.
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Abstract
Radiation is a mainstay of lung cancer treatment; however, resistance frequently develops. Identifying novel therapeutic targets to increase radiation sensitivity is crucial. S6K1 is a serine/threonine kinase known to regulate protein translation which is associated with radioresistance, but the mechanisms involved are unknown. We proposed to determine whether S6K1 promotes radioresistance by regulating DNA repair in lung cancer. Colony formation, protein expression and proliferation were assessed. S6K1 was modulated pharmacologically by either PF-4708671 or genetically by Crispr-Cas9. Higher radioresistance levels in lung cancer cells were associated with lower phosphoactivation of MRN complex members, a key activator of radiation-induced DNA repair signaling. We also found lower levels of p-ATM, a target of the MRN complex, in more radioresistant cells, which was associated with a lower expression of γ-H2AX cafter radiation. Further, genetic and pharmacological S6K1 targeting sensitized lung cancer cells to low doses of radiation (
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