ArticleOncoTargets and therapy2018
NFATC2 is a novel therapeutic target for colorectal cancer stem cells.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Harmine Hydrochloride fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Nuclear factor of activated T cells as a driver of tumor progression and a target for precision therapy.Animal models and experimental medicine · 2026Review
- NFATC2/SERPINE1/JAK3/STAT3 signaling feedback loop in gastric cancer: immune evasion and anti-PD-1 resistance.Cell biology and toxicology · 2025Article
- Hippo/YAP signaling pathway in colorectal cancer: regulatory mechanisms and potential drug exploration.Frontiers in oncology · 2025Review
- Lynch syndrome-associated and sporadic microsatellite unstable colorectal cancers: different patterns of clonal evolution yield highly similar tumours.Human molecular genetics · 2024Article
- The Dual Role of the NFATc2/galectin-9 Axis in Modulating Tumor-Initiating Cell Phenotypes and Immune Suppression in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Sarcomas with EWSR1::Non-ETS Fusion (EWSR1::NFATC2 and EWSR1::PATZ1).Surgical pathology clinics · 2024Review
- Article
- Identification of Piezo1 as a potential target for therapy of colon cancer stem-like cells.Discover oncology · 2023Article
- Functional analysis ofFrontiers in medicine · 2023Article
- Evaluation of Expression Levels of NFATc2 and PPARG Genes Two Effector Elements of WNT Pathway in Non-Small Cell Lung Carcinoma.Advanced biomedical research · 2023Article
- Chronic Alcohol Exposure Promotes Cancer Stemness and Glycolysis in Oral/Oropharyngeal Squamous Cell Carcinoma Cell Lines by Activating NFAT Signaling.International journal of molecular sciences · 2022Article
- MethReg: estimating the regulatory potential of DNA methylation in gene transcription.Nucleic acids research · 2022Article
- YAP promotes self-renewal of gastric cancer cells by inhibiting expression of L-PTGDS and PTGDR2.International journal of clinical oncology · 2020Article
- Article
- EWSR1/FUS-NFATc2 rearranged round cell sarcoma: clinicopathological series of 4 cases and literature review.Human pathology · 2019Review
- Mechanobiology of Cancer Stem Cells and Their Niche.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2019Review
- PTPRU, As A Tumor Suppressor, Inhibits Cancer Stemness By Attenuating Hippo/YAP Signaling Pathway.OncoTargets and therapy · 2019Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer stem cells (CRC-SCs) contribute to the initiation and progression of colorectal cancer (CRC). However, the underlying mechanisms for the propagation of CRC-SCs have remained elusive. PURPOSE: The objective of this study was to study the role of NFATC2 in maintenance of the stemness in CRC-SCs.
methodThe expression levels of mRNA and protein were determined by qRT-PCR and western-blot, respectively. CRC-SCs were isolated by spheroid formation assay and flowcytometry. The sphere-forming and self-renewal abilities of CRC-SCs were determined by spheroid formation assay. The tumorigenicity of CRC-SCs was determined by cell-derived xenograft model. Gene manipulation was performed by lentivirus-mediated delivery system.
resultsWe first found that NFATC2 is upregulated in primary CRC-SCs. Overexpression of NFATC2 promotes self-renewal and the expression of stem cell markers of CRC-SCs. Conversely, knockdown of NFATC2 attenuates stem cell-like properties of CRC-SCs. Mechanistic analysis indicated that NFATC2 upregulates the expression of AJUBA, downregulates the phosphorylation level of YAP, and therefore activates the transcriptional activities of YAP and promotes the stemness of CRC-SCs.
conclusionOur findings demonstrate NFATC2 as an oncogene that can promote the stemness of CRC-SCs. This work suggests a novel therapeutic strategy against CRC caused by aberrant expression of NFATC2.
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