ArticleMolecular cancer2022
CREB3L1 promotes tumor growth and metastasis of anaplastic thyroid carcinoma by remodeling the tumor microenvironment.
Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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74 citing papers in PubMed, 97 citations in OpenAlex.
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- The Application of 3D Cell Culture in Thyroid Cancer.Annals of biomedical engineering · 2026Review
- CCR7-PERK-CREB3L1 signaling mediates tumor-associated macrophages-derived SPP1 promotion of oral squamous cell carcinoma.Communications biology · 2026Article
- Matrix stiffness induced CREB3L1 activation contributed to skin fibrosis through calcium influx triggered endoplasmic reticulum stress.Cellular and molecular life sciences : CMLS · 2026Article
- MicroRNA-23b: Roles, functions and mechanisms in tumor.Genes & diseases · 2026Review
- Distinct multiplex immunofluorescence-based immune and stromal marker expression profile of subcutaneously metastatic SMARCA4-deficient undifferentiated thoracic tumor: a case report.Translational lung cancer research · 2026Article
- Spatially resolved single cell analysis suggests an APOE NCF1 associated immunosuppressive niche and its prognostic signature in thyroid cancer.Discover oncology · 2026Article
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- Preliminary study on ketone body metabolism in anaplastic thyroid cancer.European thyroid journal · 2026Article
- Decoding the Cellular Heterogeneity and Malignant Progression of Human Penile Squamous Cell Carcinoma by Single-Cell RNA Sequencing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cancer Stemness and Dedifferentiation in Anaplastic Thyroid Carcinoma: Insights into a Multigenic, Microenvironmental Network and the Role of CD44.Biomedicines · 2026Review
- Pan-cancer analysis reveals molecular signatures for predicting matrix stiffness in solid tumors.International journal of cancer · 2026Article
- Tumor microenvironment-guided targeted and immunotherapy in anaplastic thyroid cancer: a literature review from preclinical models to clinical translation.Translational cancer research · 2026Review
- State of the Art on Thyroid Cancer Biology and Oncology.Biomedicines · 2026Review
- Lipid Metabolism-Related Genes Define Prognosis and Therapeutic Targets in Thyroid Cancer.International journal of genomics · 2026Article
- CXCL8/SDC1 axis mediates tumor stem cell interactions to drive remote transfer in thyroid cancer.Journal of pharmaceutical analysis · 2026Article
- Roles and subtypes of cancer-associated fibroblasts (CAFs) in thyroid cancer.American journal of cancer research · 2026Review
- TSH suppression therapy from an individualized perspective: from mechanism to clinical decision-making.Frontiers in endocrinology · 2026Review
14 more citing papers are in PubMed but not listed here.
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20 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic thyroid carcinoma (ATC) is an extremely malignant type of endocrine cancer frequently accompanied by extrathyroidal extension or metastasis through mechanisms that remain elusive. We screened for the CREB3 transcription-factor family in a large cohort, consisting of four microarray datasets. This revealed that CREB3L1 was specifically up regulated in ATC tissues and negatively associated with overall survival of patients with thyroid cancer. Consistently, high expression of CREB3L1 was negatively correlated with progression-free survival in an independent cohort. CREB3L1 knockdown dramatically attenuated invasion of ATC cells, whereas overexpression of CREB3L1 facilitated the invasion of papillary thyroid carcinoma (PTC) cells. Loss of CREB3L1 inhibited metastasis and tumor growth of ATC xenografts in zebrafish and nude mouse model. Single-cell RNA-sequencing analysis revealed that CREB3L1 expression gradually increased during the neoplastic progression of a thyroid follicular epithelial cell to an ATC cell, accompanied by the activation of the extracellular matrix (ECM) signaling. CREB3L1 knockdown significantly decreased the expression of collagen subtypes in ATC cells and the fibrillar collagen in xenografts. Due to the loss of CREB3L1, ATC cells were unable to activate alpha-smooth muscle actin (α-SMA)-positive cancer-associated fibroblasts (CAFs). After CREB3L1 knockdown, the presence of CAFs inhibited the growth of ATC spheroids and the metastasis of ATC cells. Further cytokine array screening showed that ATC cells activated α-SMA-positive CAFs through CREB3L1-mediated IL-1α production. Moreover, KPNA2 mediated the nuclear translocation of CREB3L1, thus allowing it to activate downstream ECM signaling. These results demonstrate that CREB3L1 maintains the CAF-like property of ATC cells by activating the ECM signaling, which remodels the tumor stromal microenvironment and drives the malignancy of ATC.
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