ArticleOncotarget2015
Identification of thyroid tumor cell vulnerabilities through a siRNA-based functional screening.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- COPZ1 depletion induces cell death through different mechanisms in in vitro murine models of thyroid cancer.European thyroid journal · 2026Article
- A Robust siRNA Screening Approach with Optimized Conditions for Large-Scale Transfection in Multiple Human Cancer Cell Lines.Methods in molecular biology (Clifton, N.J.) · 2025Article
- COPZ1: an example of non-oncogene addiction in human tumors.Frontiers in pharmacology · 2025Review
- CDK4 phosphorylation status and rational use for combining CDK4/6 and BRAF/MEK inhibition in advanced thyroid carcinomas.Frontiers in endocrinology · 2023Article
- Article
- Discovery and Characterization of a Novel MASTL Inhibitor MKI-2 Targeting MASTL-PP2A in Breast Cancer Cells and Oocytes.Pharmaceuticals (Basel, Switzerland) · 2021Article
- PP2A-B55 Holoenzyme Regulation and Cancer.Biomolecules · 2020Review
- The Greatwall kinase safeguards the genome integrity by affecting the kinome activity in mitosis.Oncogene · 2020Article
- MASTL: A novel therapeutic target for Cancer Malignancy.Cancer medicine · 2020Review
- A paralog-specific role of COPI vesicles in the neuronal differentiation of mouse pluripotent cells.Life science alliance · 2020Article
- AKT Regulates Mitotic Progression of Mammalian Cells by Phosphorylating MASTL, Leading to Protein Phosphatase 2A Inactivation.Molecular and cellular biology · 2020Article
- Review
- MKI-1, a Novel Small-Molecule Inhibitor of MASTL, Exerts Antitumor and Radiosensitizer Activities Through PP2A Activation in Breast Cancer.Frontiers in oncology · 2020Article
- Metabolomic Alterations in Thyrospheres and Adherent Parental Cells in Papillary Thyroid Carcinoma Cell Lines: A Pilot Study.International journal of molecular sciences · 2018Article
- MASTL inhibition promotes mitotic catastrophe through PP2A activation to inhibit cancer growth and radioresistance in breast cancer cells.BMC cancer · 2018Article
- Therapeutic relevance of the PP2A-B55 inhibitory kinase MASTL/Greatwall in breast cancer.Cell death and differentiation · 2018Article
- The Oncogenic Functions of MASTL Kinase.Frontiers in cell and developmental biology · 2018Review
- Cell cycle-dependent regulation of Greatwall kinase by protein phosphatase 1 and regulatory subunit 3B.The Journal of biological chemistry · 2017Article
- Thyrospheres from B-CPAP Cell Line withJournal of Cancer · 2017Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of thyroid carcinoma is rapidly increasing. Although generally associated with good prognosis, a fraction of thyroid tumors are not cured by standard therapy and progress to aggressive forms for which no effective treatments are currently available. In order to identify novel therapeutic targets for thyroid carcinoma, we focused on the discovery of genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same degree for the viability of normal cells (non-oncogene addiction paradigm). We screened a siRNA oligonucleotide library targeting the human druggable genome in thyroid cancer BCPAP cell line in comparison with immortalized normal human thyrocytes (Nthy-ori 3-1). We identified a panel of hit genes whose silencing interferes with the growth of tumor cells, while sparing that of normal ones. Further analysis of three selected hit genes, namely Cyclin D1, MASTL and COPZ1, showed that they represent common vulnerabilities for thyroid tumor cells, as their inhibition reduced the viability of several thyroid tumor cell lines, regardless the histotype or oncogenic lesion. This work identified non-oncogenes essential for sustaining the phenotype of thyroid tumor cells, but not of normal cells, thus suggesting that they might represent promising targets for new therapeutic strategies.
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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.