ArticleCell death & disease2017
iASPP facilitates tumor growth by promoting mTOR-dependent autophagy in human non-small-cell lung cancer.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Comprehensive bioinformatics analysis and clinical validation of PPP1R13L in rectal adenocarcinoma.BMC cancer · 2026Article
- LncRNA-Gm5532 deficiency alleviates bone resorption by inhibiting mitochondrial respiration through iASPP/NRF2.Cell biology and toxicology · 2026Article
- [Expression Characteristics and Prognostic Study of PPP1R13L in Brain Metastases of Lung Adenocarcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
- Integrated systems biology reveals an 8-gene signature predicting early-stage lung adenocarcinoma progression and patient survival.Scientific reports · 2025Article
- Review
- PPP1R13L drives cervical cancer progression by suppressing p63-mediated PTEN transcription.Cellular and molecular life sciences : CMLS · 2025Article
- Nucleotide excision repair gene polymorphisms and hepatoblastoma susceptibility in Eastern Chinese children: A five-center case-control study.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024Article
- Inhibitor of apoptosis stimulating protein of p53 protects against MPPMetabolic brain disease · 2024Article
- Molecular Mechanisms of Autophagy in Cancer Development, Progression, and Therapy.Biomedicines · 2022Review
- Role and mechanisms of autophagy in lung metabolism and repair.Cellular and molecular life sciences : CMLS · 2021Review
- Demethylation ofOncology letters · 2020Article
- Elevated Expression of Inhibitor of Apoptosis-stimulating Protein of p53 (iASPP) and Methyltransferase-like 3 (METTL3) Correlate with Poor Prognosis in FIGO Ib1-IIa Squamous Cell Cervical Cancer.Journal of Cancer · 2020Article
- Overexpression of iASPP is required for autophagy in response to oxidative stress in choriocarcinoma.BMC cancer · 2019Article
- iASPP mediates p53 selectivity through a modular mechanism fine-tuning DNA recognition.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Pharmacological inhibition of autophagy by 3-MA attenuates hyperuricemic nephropathy.Clinical science (London, England : 1979) · 2018Article
- Interplay between P-Glycoprotein Expression and Resistance to Endoplasmic Reticulum Stressors.Molecules (Basel, Switzerland) · 2018Review
- Autophagy and pulmonary disease.Therapeutic advances in respiratory diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy serves a critical function in the pathogenesis, response to therapy and clinical outcome in cancers. Although a recent report showed a role of iASPP in suppressing autophagy, its potential activity as a regulator of autophagy has not been investigated in lung cancer. Here we investigated the potential function and molecular mechanism of iASPP in mediating autophagy in human non-small-cell lung cancer. Our data suggested that forced expression of iASPP triggered autophagic flux, while inhibition of iASPP suppressed autophagy at the autophagsome formation stage in vitro. Furthermore, in vivo overexpression of iASPP in SCID/NOD mice promoted tumorigenesis and autophagy, with an increase in the conversion from LC3-I to LC3-II. The effects of iASPP were mediated through activation of mTOR pathway. Finally, cytoplasmic iASPP expression was upregulated in lung cancer patients, and was identified as an independent poor prognostic factor for lung cancer-specific death in patient samples. Taken together, our data showed that iASPP could promote tumor growth by increasing autophagic flux, and iASPP could serve as a poor prognostic factor and a potential therapeutic target in lung cancer.
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.