ArticleCommunications biology2021
Targeting therapy-resistant lung cancer stem cells via disruption of the AKT/TSPYL5/PTEN positive-feedback loop.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 27 citations in OpenAlex.
- Artificial Intelligence-Based In Silico Evaluation of the Pharmacological Potential and In Vitro Anti-Malignancy Effect in the Human Glioblastoma Cell Line of the Hydrate of the Coumarin Compound Meranzin Originating From the Edible Macroalga (Food science & nutrition · 2026Article
- TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma.Cell death & disease · 2025Article
- In silico-based analysis and in vitro experiments identify SIGMAR1 as a potential marker of putative lung cancer stem cells.Discover oncology · 2025Article
- Elucidating the Role of FASN in Lung Cancer Stem Cells in Sensitive and Resistant EGFR-Mutated Non-Small Cell Lung Cancer Cells.Lung Cancer (Auckland, N.Z.) · 2025Article
- Navigating the Molecular Signaling: Deciphering Cancer Stem Cell Self-Renewal Pathways.International journal of molecular and cellular medicine · 2025Review
- The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.The Journal of biological chemistry · 2024Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- PLAU promotes growth and attenuates cisplatin chemosensitivity in ARID1A-depleted non-small cell lung cancer through interaction with TM4SF1.Biology direct · 2024Article
- Insights into the Cellular Localization and Functional Properties of TSPYL5 Protein.International journal of molecular sciences · 2023Article
- 3D cell subculturing pillar dish for pharmacogenetic analysis and high-throughput screening.Materials today. Bio · 2023Article
- Novel Synthetic Derivative of Renieramycin T Right-Half Analog Induces Apoptosis and Inhibits Cancer Stem Cells via Targeting the Akt Signal in Lung Cancer Cells.International journal of molecular sciences · 2023Article
- Mitochondria in Cancer Stem Cells: From an Innocent Bystander to a Central Player in Therapy Resistance.Stem cells and cloning : advances and applications · 2023Review
- Protein tyrosine kinase inhibitor resistance in malignant tumors: molecular mechanisms and future perspective.Signal transduction and targeted therapy · 2022Review
- Clinical Application Perspectives of Lung Cancers 3D Tumor Microenvironment Models for In Vitro Cultures.International journal of molecular sciences · 2022Review
- ALDH1: A potential therapeutic target for cancer stem cells in solid tumors.Frontiers in oncology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) are regarded as essential targets to overcome tumor progression and therapeutic resistance; however, practical targeting approaches are limited. Here, we identify testis-specific Y-like protein 5 (TSPYL5) as an upstream regulator of CSC-associated genes in non-small cell lung cancer cells, and suggest as a therapeutic target for CSC elimination. TSPYL5 elevation is driven by AKT-dependent TSPYL5 phosphorylation at threonine-120 and stabilization via inhibiting its ubiquitination. TSPYL5-pT120 also induces nuclear translocation and functions as a transcriptional activator of CSC-associated genes, ALDH1 and CD44. Also, nuclear TSPYL5 suppresses the transcription of PTEN, a negative regulator of PI3K signaling. TSPYL5-pT120 maintains persistent CSC-like characteristics via transcriptional activation of CSC-associated genes and a positive feedback loop consisting of AKT/TSPYL5/PTEN signaling pathway. Accordingly, elimination of TSPYL5 by inhibiting TSPYL5-pT120 can block aberrant AKT/TSPYL5/PTEN cyclic signaling and TSPYL5-mediated cancer stemness regulation. Our study suggests TSPYL5 be an effective target for therapy-resistant 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.