ArticleMolecular and cellular biology2017
mTORC1 and -2 Coordinate Transcriptional and Translational Reprogramming in Resistance to DNA Damage and Replicative Stress in Breast Cancer Cells.
Article in Molecular and cellular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Compensatory evolution to DNA replication stress is robust to nutrient availability.Molecular systems biology · 2025Article
- Visualization of breast cancer-related protein synthesis from the perspective of bibliometric analysis.European journal of medical research · 2023Article
- Therapeutic targeting of histone lysine demethylase KDM4B blocks the growth of castration-resistant prostate cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Inhibition of the Translation Initiation Factor eIF4A Enhances Tumor Cell Radiosensitivity.Molecular cancer therapeutics · 2022Article
- DNA-PK promotes activation of the survival kinase AKT in response to DNA damage through an mTORC2-ECT2 pathway.Science signaling · 2022Article
- RAD21 Confers Poor Prognosis and Affects Ovarian Cancer Sensitivity to Poly(ADP-Ribose)Polymerase Inhibitors Through DNA Damage Repair.Frontiers in oncology · 2022Article
- Chemical Biology Screening Identifies a Vulnerability to Checkpoint Kinase Inhibitors in TSC2-Deficient Renal Angiomyolipomas.Frontiers in oncology · 2022Article
- Narrative review of emerging roles for AKT-mTOR signaling in cancer radioimmunotherapy.Annals of translational medicine · 2021Review
- Translation Initiation Machinery as a Tumor Selective Target for Radiosensitization.International journal of molecular sciences · 2021Review
- AXL Inhibition Induces DNA Damage and Replication Stress in Non-Small Cell Lung Cancer Cells and Promotes Sensitivity to ATR Inhibitors.Molecular cancer research : MCR · 2021Article
- H3K4me2 regulates the recovery of protein biosynthesis and homeostasis following DNA damage.Nature structural & molecular biology · 2020Article
- Targeting the PI3K/mTOR Pathway Augments CHK1 Inhibitor-Induced Replication Stress and Antitumor Activity in High-Grade Serous Ovarian Cancer.Cancer research · 2020Article
- Targeting the PI3K pathway and DNA damage response as a therapeutic strategy in ovarian cancer.Cancer treatment reviews · 2020Review
- Torin2 Exploits Replication and Checkpoint Vulnerabilities to Cause Death of PI3K-Activated Triple-Negative Breast Cancer Cells.Cell systems · 2020Article
- Next-generation RNA sequencing of FFPE subsections reveals highly conserved stromal reprogramming between canine and human mammary carcinoma.Disease models & mechanisms · 2019Article
- Article
- The nucleolus, an ally, and an enemy of cancer cells.Histochemistry and cell biology · 2018Review
- RIVET: comprehensive graphic user interface for analysis and exploration of genome-wide translatomics data.BMC genomics · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
mTOR coordinates growth signals with metabolic pathways and protein synthesis and is hyperactivated in many human cancers. mTOR exists in two complexes: mTORC1, which stimulates protein, lipid, and ribosome biosynthesis, and mTORC2, which regulates cytoskeleton functions. While mTOR is known to be involved in the DNA damage response, little is actually known regarding the functions of mTORC1 compared to mTORC2 in this regard or the respective impacts on transcriptional versus translational regulation. We show that mTORC1 and mTORC2 are both required to enact DNA damage repair and cell survival, resulting in increased cancer cell survival during DNA damage. Together mTORC1 and -2 enact coordinated transcription and translation of protective cell cycle and DNA replication, recombination, and repair genes. This coordinated transcriptional-translational response to DNA damage was not impaired by rapalog inhibition of mTORC1 or independent inhibition of mTORC1 or mTORC2 but was blocked by inhibition of mTORC1/2. Only mTORC1/2 inhibition reversed cancer cell resistance to DNA damage and replicative stress and increased tumor cell killing and tumor control by DNA damage therapies in animal models. When combined with DNA damage, inhibition of mTORC1/2 blocked transcriptional induction more strongly than translation of DNA replication, survival, and DNA damage response mRNAs.
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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.