ArticleCancer management and research2020
CUB Domain-Containing Protein-1 Promotes Proliferation, Migration and Invasion in Cervical Cancer Cells.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- High CDCP1 Expression Reflects Immune and Stromal Remodeling and Oncogenic Signaling in Pancreatic Ductal Adenocarcinoma.World journal of oncology · 2026Article
- CDCP1 promotes the malignant phenotypes of nasopharyngeal carcinoma via the Wnt/β-catenin signaling pathway.BMC biotechnology · 2025Article
- Article
- Targeting CDCP1 boost CD8+ T cells-mediated cytotoxicity in cervical cancer via the JAK/STAT signaling pathway.Journal for immunotherapy of cancer · 2024Article
- The effect of inflammatory cytokines on the risk of hypertrophic scar: a mendelian randomization study.Archives of dermatological research · 2024Article
- Molecular mechanism by which CDCP1 promotes proneural-mesenchymal transformation in primary glioblastoma.Cancer cell international · 2022Article
- hsa_circ_0005358 suppresses cervical cancer metastasis by interacting with PTBP1 protein to destabilize CDCP1 mRNA.Molecular therapy. Nucleic acids · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeEmerging evidence have revealed significant contributions of CUB domain-containing protein-1 (CDCP1) in tumorigenesis, including colon, renal, ovarian, pancreatic, prostate and breast cancers. However, the roles of CDCP1 in cervical cancer (CC) still remain elusive. MATERIALS AND
methodsQuantitative reverse transcription polymerase chain reaction, immunohistochemistry and Western blotting were used to confirm the expression of CDCP1 in CC tissues compared with matched non-tumor tissues. In vitro, gain-of-function and loss-of-function studies were used to investigate the biological function and underlying mechanism of CDCP1 in cervical carcinogenesis. Furthermore, tumor growth was evaluated using a xenogenous subcutaneously implant model of CC cells in vivo.
resultsHere, we confirmed that CDCP1 was significantly increased in human CC both in mRNA and in protein levels compared to normal cervical tissues. Furthermore, we demonstrated that increased CDCP1 expression promotes proliferation, migration, invasion and mediates the epithelial-to-mesenchymal transition phenotype in HeLa and C33A cells. Also, CDCP1 knockdown reverses all the effects of enhanced CDCP1 on cell behavior in SiHa and Caski cells. Importantly, the suppressive expression of CDCP1 repressed tumor growth in a mouse xenograft model of CC.
conclusionIn summary, our current study results provide novel insights into the role of CDCP1 in CC progression. Potentially, CDCP1 might serve as a diagnostic biomarker and a novel therapeutic target for CC.
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