ArticleFrontiers in cell and developmental biology2021
Follistatin-Like 3 Enhances Invasion and Metastasis via β-Catenin-Mediated EMT and Aerobic Glycolysis in Colorectal Cancer.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- ZNF454-FSTL3 axis inhibits colorectal cancer progression by inhibiting HIF-1α-mediated glycolysis in hypoxia.Journal of gastrointestinal oncology · 2025Article
- A novel anoikis related gene prognostic model for colorectal cancer based on single cell sequencing and bulk transcriptome analyses.Scientific reports · 2025Article
- BMP signalling in colorectal cancer: losing the yin to WNTs yang.The Journal of pathology · 2025Review
- Integrated analysis of shared gene expression signatures and immune microenvironment heterogeneity in type 2 diabetes mellitus and colorectal cancer.Scientific reports · 2025Article
- Multi-Omics analysis elucidates tumor microenvironment and intratumor microbes of angiogenesis subtypes in colon cancer.World journal of gastrointestinal oncology · 2024Article
- Canonical WNT/β-catenin signaling upregulates aerobic glycolysis in diverse cancer types.Molecular biology reports · 2024Review
- FSTL3 promotes tumor immune evasion and attenuates response to anti-PD1 therapy by stabilizing c-Myc in colorectal cancer.Cell death & disease · 2024Article
- Transcriptomic and epigenetic dissection of spinal ependymoma (SP-EPN) identifies clinically relevant subtypes enriched for tumors with and without NF2 mutation.Acta neuropathologica · 2024Article
- Bioinformatic Analyses and Integrated Machine Learning to Predict prognosis and therapeutic response Based on E3 Ligase-Related Genes in colon cancer.Journal of Cancer · 2024Article
- Stroma-associated FSTL3 is a factor of calcium channel-derived tumor fibrosis.Scientific reports · 2023Article
- HES1 promotes aerobic glycolysis and cancer progression of colorectal cancer via IGF2BP2-mediated GLUT1 m6A modification.Cell death discovery · 2023Article
- Prediction of risk and clinical outcome of cuproptosis in lung squamous carcinoma.BMC pulmonary medicine · 2023Article
- Quiescent Ovarian Cancer Cells Secrete Follistatin to Induce Chemotherapy Resistance in Surrounding Cells in Response to Chemotherapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- The cytoplasmic expression of FSTL3 correlates with colorectal cancer progression, metastasis status and prognosis.Journal of cellular and molecular medicine · 2023Article
- A Prognostic Model of Angiogenesis and Neutrophil Extracellular Traps Related Genes Manipulating Tumor Microenvironment in Colon Cancer.Journal of Cancer · 2023Article
- BRD9 is an essential regulator of glycolysis that creates an epigenetic vulnerability in colon adenocarcinoma.Cancer medicine · 2023Article
- A new machine learning method for cancer mutation analysis.PLoS computational biology · 2022Article
- Elevation of ADAM12 facilitates tumor progression by enhancing metastasis and immune infiltration in gastric cancer.International journal of oncology · 2022Article
- Roles of follistatin-like protein 3 in human non-tumor pathophysiologies and cancers.Frontiers in cell and developmental biology · 2022Review
- The Role of DACT Family Members in Tumorigenesis and Tumor Progression.International journal of biological sciences · 2022Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies reported that Follistatin-like 3 (FSTL3) is abundantly expressed in several solid tumors and participate in the regulation of cell metabolism. However, the clinico-pathological significance, biological role and molecular mechanism of FSTL3 in colorectal cancer (CRC) is still unclear. Here we report that the expression level of FSTL3 in colon cancer specimens was significantly higher, compared to normal tissue and interestingly, the expression of FSTL3 was related to lymph node metastasis, tumor stage, tumor size, and intravascular emboli (IVE). As an upstream molecular event, we found that transcriptional regulation of FSTL3 was highly dependent on YAP1 de-phosphorylation events and that increased FSTL3 expression readily activated the β-Catenin pathway, which is a well-known signaling hub that promotes EMT processes and aerobic glycolysis in cancer cells. We found that elevated FSTL3 expression strongly promotes migration, invasion and metastatic formation of CRC cells by directly activating β-Catenin -mediated EMT and aerobic glycolysis. In the xenograft mouse model, FSTL3 expression was linked to increased metastatic formation of CRC cells. Together, the activation of YAP1 induces FSTL3 expression. FSTL3-mediated β-Catenin pathway activation promotes EMT and aerobic glycolysis and therefore affecting the invasive and metastatic capacity of CRC cells. The abundant FSTL3 expression is a poor prognostic factor and pharmacological targeting of YAP1 can counteract FSTL3 expression, suggesting a promising therapeutic target for anti-metastatic strategies in patients suffering from CRC.
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