ArticleFrontiers in molecular biosciences2021
Downregulation of CacyBP by CRISPR/dCas9-KRAB Prevents Bladder Cancer Progression.
Article in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Analysis of CacyBP/SIP, ERK1/2, and p38 Expression in Low- and High-Grade Papillary Urothelial Carcinoma.Cancer medicine · 2026Article
- Machine Learning Integration Framework Constructs a Lactylation-Associated Gene Signature to Improve Prognosis in Bladder Cancer.Cancer medicine · 2026Article
- Urine proteomics-based analysis identifies CHI3L1 as an immune marker and potential therapeutic target for bladder cancer.BMC cancer · 2025Article
- Integrative bioinformatics and experimental analyses identify U2SURP as a novel lactylation-related prognostic signature in esophageal carcinoma.Immunologic research · 2025Article
- Epigenetic regulation of bladder cancer in the context of aging.Frontiers in pharmacology · 2025Review
- Pan-analysis reveals CACYBP to be a novel prognostic and predictive marker for multiple cancers.American journal of translational research · 2024Article
- Blockage of CacyBP inhibits macrophage recruitment and improves anti-PD-1 therapy in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- CACYBP knockdown inhibits progression of prostate cancer via p53.Journal of cancer research and clinical oncology · 2023Article
- (Nano)platforms in bladder cancer therapy: Challenges and opportunities.Bioengineering & translational medicine · 2023Review
- Significance of Hypermethylation of Tumor-Suppressor Genes PTGER4 and ZNF43 at CpG Sites in the Prognosis of Colorectal Cancer.International journal of molecular sciences · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BCa) is a leading cause of cancer-related death in the world. CacyBP is initially described as a binding partner of calcyclin and has been shown to be involved in a wide range of cellular processes, including cell differentiation, proliferation, protein ubiquitination, cytoskeletal dynamics and tumorigenesis. In the present study, we found that CacyBP expression was significantly upregulated in BCa tissues compared with adjacent normal tissues. Moreover, its expression was negatively correlated with overall survival time. Secondly, CacyBP had higher expressions in BCa cell lines than normal urothelial cells which was consistent with the results of BCa tissues. Finally, knockdown of CacyBP by CRIPSR-dCas9-KRAB in T24 and 5,637 BCa cells inhibited cell proliferation and migration by CCK-8 assay and scratch assay, and promoted apoptosis by caspase-3/ELISA. These data elucidate that CacyBP is an important oncogene contributing to malignant behavior of BCa and provide a potentially molecular target for treatment of BCa.
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