ArticleOncogene2024
The TβRI promotes migration and metastasis through thrombospondin 1 and ITGAV in prostate cancer cells.
Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Targeting oncogenic TβRI signaling inhibits androgen-independent prostate cancer growth and metastasis.Signal transduction and targeted therapy · 2026Article
- Machine learning-guided multimodal profiling defines perturbed immune states at the time of cancer diagnosis.Briefings in bioinformatics · 2026Article
- LncRNA NKILA as a key regulator in cancer pathogenesis: insights into its mechanisms and clinical implications.Cancer cell international · 2026Review
- Growth hormone therapy promotes bone growth in idiopathic short stature children by activating the IGF-1 pathway via IGFBP2-mediated inhibition of THBS1.In vitro cellular & developmental biology. Animal · 2025Article
- Integrative analysis identifiedTranslational cancer research · 2025Article
- ITGAV as a promising diagnostic, immunological, and prognostic biomarker in pan-cancer.Scientific reports · 2025Article
- Characterizing resistant cellular states in nasopharyngeal carcinoma during EBV lytic induction.Oncogene · 2025Article
- Identification of progression markers for prostate cancer.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
TGFβ potently modifies the extracellular matrix (ECM), which is thought to favor tumor cell invasion. However, the mechanism whereby the cancer cells employ the ECM proteins to facilitate their motility is largely unknown. In this study we used RNA-seq and proteomic analysis to examine the proteins secreted by castration-resistant prostate cancer (CRPC) cells upon TGFβ treatment and found that thrombospondin 1 (THBS1) was observed to be one of the predominant proteins. The CRISPR Cas9, or siRNA techniques was used to downregulate TGFβ type I receptor (TβRI) to interfere with TGFβ signaling in various cancer cells in vitro. The interaction of ECM proteins with the TβRI in the migratory prostate cancer cells in response to TGFβ1 was demonstrated by several different techniques to reveal that THBS1 mediates cell migration by interacting with integrin subunit alpha V (ITGAV) and TβRI. Deletion of TβRI or THBS1 in cancer cells prevented their migration and invasion. THBS1 belongs to a group of tumorigenic ECM proteins induced via TGFβ signaling in CRPC cells, and high expression of THBS1 in human prostate cancer tissues correlated with the degree of malignancy. TGFβ-induced production of THBS1 through TβRI facilitates the invasion and metastasis of CRPC cells as shown in vivo xenograft animal experiments.
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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 Socratic graph.