ArticleThoracic cancer2023
Carboxypeptidase vitellogenic like facilitates resistance to CDK4/6 inhibitors in breast cancer.
Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 4 citations in OpenAlex.
- Multi-cohort integration and machine learning identify CPVL as a novel oncogenic driver in gastric cancer.Discover oncology · 2026Article
- A Prognostic Riskscore Model Related toInternational journal of genomics · 2025Article
- Dissecting gastric cancer heterogeneity and exploring therapeutic strategies using bulk and single-cell transcriptomic analysis and experimental validation of tumor microenvironment and metabolic interplay.Frontiers in pharmacology · 2024Article
- Carboxypeptidase vitellogenic like facilitates resistance to CDK4/6 inhibitors in breast cancer.Thoracic cancer · 2023Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInhibitors of cyclin-dependent kinase 4 and 6 (CDK4/6) are targeted therapeutic drugs for breast cancer treatment. The mechanism of resistance to these inhibitors requires further investigation.
methodsWe used bioinformatics to screen differentially expressed genes between cells that were susceptible and resistant to CDK4/6 inhibitors. Quantitative real-time PCR (qRT-PCR) was used to identify gene expressions in different cell lines. Cell viability, colony formation, cell cycle, and apoptosis assays were used to evaluate the effect of carboxypeptidase vitellogenic like (CPVL) on breast cancer cells under the condition of CDK4/6 inhibitors. Gene set enrichment analysis (GSEA) suggested the potential regulatory pathway of CPVL in breast cancer. Xenograft formation assay was conducted in nude mice to study the role of CPVL in vivo.
resultsBased on bioinformatics analysis and qRT-PCR, CPVL was identified more abundantly in cells that were resistant than sensitive to CDK4/6 inhibitors. Overexpressed or knocked down CPVL regulated the effects of CDK4/6 inhibitors in resistant cell lines. GSEA showed that resistance might be induced by CPVL through altered phosphatase and tensin homolog (PTEN)-related pathways. Our findings showed that CPVL negatively regulates PTEN to impact the anticancer effects of CDK4/6 inhibitors in vitro and in vivo.
conclusionCPVL might be a key factor in regulating breast cancer resistance to CDK4/6 inhibitors.
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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.