ArticleOncotarget2017
TAZ induces lung cancer stem cell properties and tumorigenesis by up-regulating ALDH1A1.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- YAP and TEAD Are Transcriptional Regulators of Neuroendocrine Differentiation and Growth in Carcinoid Cells.The American journal of pathology · 2026Article
- Review
- Tissue-specific cancer stem/progenitor cells: Therapeutic implications.World journal of stem cells · 2023Review
- Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma.Brain : a journal of neurology · 2023Article
- Recurrent WWTR1 S89W mutations and Hippo pathway deregulation in clear cell carcinomas of the cervix.The Journal of pathology · 2022Article
- Liver regeneration and ethanol detoxification: A new link in YAP regulation of ALDH1A1 during alcohol-related hepatocyte damage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- ALDH1A1 in Cancers: Bidirectional Function, Drug Resistance, and Regulatory Mechanism.Frontiers in oncology · 2022Review
- The role of YAP1 in survival prediction, immune modulation, and drug response: A pan-cancer perspective.Frontiers in immunology · 2022Article
- A miR-375/YAP axis regulates neuroendocrine differentiation and tumorigenesis in lung carcinoid cells.Scientific reports · 2021Article
- lncRNACell journal · 2021Article
- SOX13 regulates cancer stem-like properties and tumorigenicity in hepatocellular carcinoma cells.American journal of cancer research · 2021Article
- The regulatory networks of the Hippo signaling pathway in cancer development.Journal of Cancer · 2021Review
- A combat with the YAP/TAZ-TEAD oncoproteins for cancer therapy.Theranostics · 2020Review
- Placenta-specific 8 is a potential novel target for osimertinib resistance in non-small cell lung cancer.Oncology letters · 2019Article
- Identification of Prolyl isomerase Pin1 as a novel positive regulator of YAP/TAZ in breast cancer cells.Scientific reports · 2019Article
- TAZ sensitizes EGFR wild-type non-small-cell lung cancer to gefitinib by promoting amphiregulin transcription.Cell death & disease · 2019Article
- Fascin induces melanoma tumorigenesis and stemness through regulating the Hippo pathway.Cell communication and signaling : CCS · 2018Article
- Review
- Review
- The Hippo Pathway: Immunity and Cancer.Cancers · 2018Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies suggest that lung cancer stem cells (CSCs) may play major roles in lung cancer. Therefore, identification of lung CSC drivers may provide promising targets for lung cancer. TAZ is a transcriptional co-activator and key downstream effector of the Hippo pathway, which plays critical roles in various biological processes. TAZ has been shown to be overexpressed in lung cancer and involved in tumorigenicity of lung epithelial cells. However, whether TAZ is a driver for lung CSCs and tumor formation in vivo is unknown. In addition, the molecular mechanism underlying TAZ-induced lung tumorigenesis remains to be determined. In this study, we provided evidence that constitutively active TAZ (TAZ-S89A) is a driver for lung tumorigenesis in vivo in mice and formation of lung CSC. Further RNA-seq and qRT-PCR analysis identified Aldh1a1, a well-established CSC marker, as critical TAZ downstream target and showed that TAZ induces Aldh1a1 transcription by activating its promoter activity through interaction with the transcription factor TEAD. Most significantly, inhibition of ALDH1A1 with its inhibitor A37 or CRISPR gene knockout in lung cancer cells suppressed lung tumorigenic and CSC phenotypes in vitro, and tumor formation in mice in vivo. In conclusion, this study identified TAZ as a novel inducer of lung CSCs and the first transcriptional activator of the stem cell marker ALDH1A1. Most significantly, we identified ALDH1A1 as a critical meditator of TAZ-induced tumorigenic and CSC phenotypes in lung cancer. Our studies provided preclinical data for targeting of TAZ-TEAD-ALDH1A1 signaling to inhibit CSC-induced lung tumorigenesis in the future.
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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.