ArticleJournal of cell communication and signaling2023
Chondroitin polymerizing factor predicts a poor prognosis and promotes breast cancer progression via the upstream TGF-β1/SMAD3 and JNK axis activation.
Article in Journal of cell communication and signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 15 citations in OpenAlex.
- CMS4 epithelial-intrinsic glycosyltransferase GALNT5 promotes tumor aggressiveness and correlates with poor survival in colorectal cancer.Scientific reports · 2026Article
- Interactions between LncRNAs and MAPK signaling pathways in the pathogenesis of breast cancer.Cancer cell international · 2025Review
- An 11-gene glycosyltransferases-related model for the prognosis of patients with bladder urothelial carcinoma: development and validation based on TCGA and GEO datasets.Translational andrology and urology · 2024Article
- Targeting chondroitin sulfate suppresses macropinocytosis of breast cancer cells by modulating syndecan-1 expression.Molecular oncology · 2024Article
- Impact of NDUFAF6 on breast cancer prognosis: linking mitochondrial regulation to immune response and PD-L1 expression.Cancer cell international · 2024Article
- MiR-214-3p overexpression-triggered chondroitin polymerizing factor (CHPF) inhibition modulates the ferroptosis and metabolism in colon cancer.The Kaohsiung journal of medical sciences · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Aberrant composition of glycans in the tumor microenvironment (TME) contributes to tumor progression and metastasis. Chondroitin polymerizing factor (CHPF) is a glycosyltransferase that catalyzes the biosynthesis of chondroitin sulfate (CS). It is also correlated to transforming growth factor-β1 (TGF-β1) expression, a crucial mediator in the interaction of cancer cells with TME. In this study, we investigated the association of CHPF expression with the clinicopathological features of breast cancer (BRCA), as well the oncogenic effect and the underling mechanisms of CHPF upon BRCA cells. We found that CHPF expression is significantly increased in human BRCA tissues, and it is positively associated with TGF-β expression (r = 0.7125). The high-expression of CHPF predicts a poor prognosis and is positively correlated with tumor mass, lymph node metastasis, clinical staging and HER-2 negative-expression. The mechanistic study revealed that it promotes BRCA cell proliferation, migration and invasion through TGF-β1-induced SMAD3 and JNK activation in vitro, JNK (SP600125) or SMAD3 (SIS3) inhibitor can remove the promotion of CHPF upon cell proliferation, migration and invasion in MDA-MB-231 cells, which is derived from triple-negative breast cancer (TNBC). Collectively, our finding suggested CHPF may function as an oncogene and is highly expressed in human BRCA tissues. Pharmacological blockade of the upstream of JNK or SMAD3 signaling may provide a novel therapeutic target for refractory TNBC patients with CHPF abnormal high-expression.
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