ReviewInternational journal of molecular sciences2013
The role of AKT/mTOR pathway in stress response to UV-irradiation: implication in skin carcinogenesis by regulation of apoptosis, autophagy and senescence.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 157 citations in OpenAlex.
- Activation of the PI3K/Akt/mTOR and MAPK Signaling Pathways in Response to Acute Solar-Simulated Light Exposure of Human Skin.Cancer prevention research (Philadelphia, Pa.) · 2015Trial
- Deciphering the Medicinal Chemistry Aspects of Akt Inhibitors for the Management of Cancer: Structure-Activity Relationship Frameworks, Landscapes, and Optimization Approaches.Chemistry & biodiversity · 2026Review
- AHR: The Overlooked Mediator in SkincareBridging Environmental Sensing and Skin Physiology.Environment & health (Washington, D.C.) · 2026Review
- Nanoparticles-based phototherapy systems: molecular mechanisms and clinical applications.Signal transduction and targeted therapy · 2026Review
- Subcytotoxic Exposure to Avobenzone and Ethylhexyl Salicylate Induces microRNA Modulation and Stress-Responsive PI3K/AKT and MAPK Signaling in Differentiated SH-SY5Y Cells.International journal of molecular sciences · 2026Article
- UVB-induced genotoxic stress activates the DNA damage response and innate immune pathways in sea urchin coelomocytes.Frontiers in immunology · 2026Article
- Autophagy and mitophagy in dermatological disease: a comprehensive review from molecular pathways to therapeutic frontiers.Biology direct · 2025Review
- Okanin Attenuates Mitochondrial Dysfunction and Apoptosis in UVA-Induced HaCaT Cells by Mitophagy Through SIRT3 Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- The Mechanism of Protective Action of Plant-Derived Squalane (2,6,10,15,19,23-Hexamethyltetracosane) Against UVA Radiation-Induced Apoptosis in Human Dermal Fibroblasts.Antioxidants (Basel, Switzerland) · 2025Article
- Attenuation of brucine action on DMBA/TPA-induced skin cancer by PI3K/Akt/mTOR signaling.Journal of molecular histology · 2025Article
- Neutrophil Extracellular Traps in Sepsis and Sepsis-Related Organ Dysfunction.ImmunoTargets and therapy · 2025Review
- P53 and the Ultraviolet Radiation-Induced Skin Response: Finding the Light in the Darkness of Triggered Carcinogenesis.Cancers · 2024Review
- Effects of Resveratrol on Nonmelanoma Skin Cancer (NMSC): A Comprehensive Review.Food science & nutrition · 2024Review
- AMPK activation eliminates senescent cells in diabetic wound by inducing NCOA4 mediated ferritinophagy.Molecular medicine (Cambridge, Mass.) · 2024Article
- Melatonin/Sericin Wound Healing Patches: Implications for Melanoma Therapy.International journal of molecular sciences · 2024Review
- Environmental pollutants and phosphoinositide signaling in autoimmunity.Journal of hazardous materials · 2024Review
- Article
- β-endorphin suppresses ultraviolet B irradiation-induced epidermal barrier damage by regulating inflammation-dependent mTORC1 signaling.Scientific reports · 2023Article
- Exploring Nanocarriers as Treatment Modalities for Skin Cancer.Molecules (Basel, Switzerland) · 2023Review
- Proteomics analysis of human breast milk by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) coupled with mass spectrometry to assess breast cancer risk.Electrophoresis · 2023Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of DNA damage by UVB and UVA radiation may generate mutations and genomic instability leading to carcinogenesis. Therefore, skin cells being repeatedly exposed to ultraviolet (UV) light have acquired multilayered protective mechanisms to avoid malignant transformation. Besides extensive DNA repair mechanisms, the damaged skin cells can be eliminated by induction of apoptosis, which is mediated through the action of tumor suppressor p53. In order to prevent the excessive loss of skin cells and to maintain the skin barrier function, apoptotic pathways are counteracted by anti-apoptotic signaling including the AKT/mTOR pathway. However, AKT/mTOR not only prevents cell death, but is also active in cell cycle transition and hyper-proliferation, thereby also counteracting p53. In turn, AKT/mTOR is tuned down by the negative regulators being controlled by the p53. This inhibition of AKT/mTOR, in combination with transactivation of damage-regulated autophagy modulators, guides the p53-mediated elimination of damaged cellular components by autophagic clearance. Alternatively, p53 irreversibly blocks cell cycle progression to prevent AKT/mTOR-driven proliferation, thereby inducing premature senescence. Conclusively, AKT/mTOR via an extensive cross talk with p53 influences the UV response in the skin with no black and white scenario deciding over death or survival.
Indexed as
Identifiers
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.