ArticleMolecular pharmacology2015
Yet another function of p53--the switch that determines whether radiation-induced autophagy will be cytoprotective or nonprotective: implications for autophagy inhibition as a therapeutic strategy.
Article in Molecular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 48 citations in OpenAlex.
- Corylin inhibits liver cancer cell growth through the endogenous apoptosis and mitophagy.Translational cancer research · 2026Article
- Autophagy-dependent sensitization effects of PARP inhibitors on recurrent nasopharyngeal carcinoma treated with carbon ion and photon irradiation.Acta biochimica et biophysica Sinica · 2025Article
- An overview of autophagy inhibition as a potential clinical strategy in cancer therapy.Molecular pharmacology · 2025Review
- Autophagy is the main driver of radioresistance of HNSCC cells in mild hypoxia.Journal of cellular and molecular medicine · 2024Article
- The role of autophagy in hypoxia-induced radioresistance.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023Review
- Article
- Of the many cellular responses activated by TP53, which ones are critical for tumour suppression?Cell death and differentiation · 2022Review
- Is Autophagy Always a Barrier to Cisplatin Therapy?Biomolecules · 2022Review
- Article
- The BET inhibitor/degrader ARV-825 prolongs the growth arrest response to Fulvestrant + Palbociclib and suppresses proliferative recovery in ER-positive breast cancer.Frontiers in oncology · 2022Article
- Role of lysosomes in physiological activities, diseases, and therapy.Journal of hematology & oncology · 2021Review
- Is targeting autophagy mechanism in cancer a good approach? The possible double-edge sword effect.Cell & bioscience · 2021Review
- P53-regulated autophagy and its impact on drug resistance and cell fate.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Immune Response: A Missed Opportunity Between Vitamin D and Radiotherapy.Frontiers in cell and developmental biology · 2021Review
- The Roles of Autophagy and Senescence in the Tumor Cell Response to Radiation.Radiation research · 2020Review
- Autophagy in cancers including brain tumors: role of MicroRNAs.Cell communication and signaling : CCS · 2020Review
- Influence of nonprotective autophagy and the autophagic switch on sensitivity to cisplatin in non-small cell lung cancer cells.Biochemical pharmacology · 2020Article
- Studies of Non-Protective Autophagy Provide Evidence that Recovery from Therapy-Induced Senescence is Independent of Early Autophagy.International journal of molecular sciences · 2020Article
- Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The influence of autophagy inhibition on radiation sensitivity was studied in human breast, head and neck, and non-small cell lung cancer cell lines, in cell lines that were either wild type or mutant/null in p53, and in cells where p53 was inducible or silenced. Whereas ionizing radiation promoted autophagy in all tumor cell lines studied, pharmacological inhibition of autophagy and/or genetic silencing of autophagy genes failed to influence sensitivity to radiation in p53 mutant Hs578t breast tumor cells, HN6 head and neck tumor cells, and H358 non-small cell lung cancer cells. The requirement for functional p53 in the promotion of cytoprotective autophagy by radiation was confirmed by the observation that radiation-induced autophagy was nonprotective in p53 null H1299 cells but was converted to the cytoprotective form with induction of p53. Conversely, whereas p53 wild-type HN30 head and neck cancer cells did show sensitization to radiation upon autophagy inhibition, HN30 cells in which p53 was knocked down using small hairpin RNA failed to be sensitized by pharmacological autophagy inhibition. Taken together, these findings indicate that radiation-induced autophagy can be either cytoprotective or nonprotective, a functional difference related to the presence or absence of function p53. Alternatively, these findings could be interpreted to suggest that whereas radiation can induce autophagy independent of p53 status, inhibition of autophagy promotes enhanced radiation sensitivity through a mechanism that requires functional p53. These observations are likely to have direct implications with respect to clinical efforts to modulate the response of malignancies to radiation through autophagy inhibition.
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.