ArticleCell cycle (Georgetown, Tex.)2014
CAPER, a novel regulator of human breast cancer progression.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 56 citations in OpenAlex.
- Breast cancer genomic subtype-specific copy number alterations in metastases.Scientific reports · 2026Article
- RNA-binding proteins as therapeutic targets in cancer.RNA biology · 2025Review
- RBM39 Promotes Base Excision Repair to Facilitate the Progression of HCC by Stabilising OGG1 mRNA.Cell proliferation · 2025Article
- RNA-binding motif protein RBM39 enhances the proliferation of gastric cancer cells by facilitating an oncogenic splicing switch in MRPL33.Acta pharmacologica Sinica · 2025Article
- Recent advances in anticancer mechanisms of molecular glue degraders: focus on RBM39-dgrading synthetic sulfonamide such as indisulam, E7820, tasisulam, and chloroquinoxaline sulfonamide.Genes & genomics · 2024Review
- Targeting RBM39 through indisulam induced mis-splicing of mRNA to exert anti-cancer effects in T-cell acute lymphoblastic leukemia.Journal of experimental & clinical cancer research : CR · 2024Article
- RBM39 is a potential prognostic biomarker with functional significance in hepatocellular carcinoma.Translational cancer research · 2024Article
- Inflammation as a driver of hematological malignancies.Frontiers in oncology · 2024Review
- Indisulam synergizes with melphalan to inhibit Multiple Myeloma malignancy via targeting TOP2A.PloS one · 2024Article
- The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress.Nucleic acids research · 2022Article
- Systematic pan-cancer analysis identifies RBM39 as an immunological and prognostic biomarker.Journal of cellular and molecular medicine · 2022Article
- The Role of RNA-Binding Proteins in Hematological Malignancies.International journal of molecular sciences · 2022Review
- RNA-binding protein 39: a promising therapeutic target for cancer.Cell death discovery · 2021Review
- Defects in Emerin-Nucleoskeleton Binding Disrupt Nuclear Structure and Promote Breast Cancer Cell Motility and Metastasis.Molecular cancer research : MCR · 2021Article
- Development of CAPER peptides for the treatment of triple negative breast cancer.Cell cycle (Georgetown, Tex.) · 2020Article
- U2AFEMBO reports · 2019Article
- CAPER as a therapeutic target for triple negative breast cancer.Oncotarget · 2018Article
- PUF60-activated exons uncover altered 3' splice-site selection by germline missense mutations in a single RRM.Nucleic acids research · 2018Article
- Distinct prostate cancer-related mRNA cargo in extracellular vesicle subsets from prostate cell lines.BMC cancer · 2017Article
- UHM-ULM interactions in the RBM39-U2AF65 splicing-factor complex.Acta crystallographica. Section D, Structural biology · 2016Article
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CAPER is an estrogen receptor (ER) co-activator that was recently shown to be involved in human breast cancer pathogenesis. Indeed, we reported increased expression of CAPER in human breast cancer specimens. We demonstrated that CAPER was undetectable or expressed at relatively low levels in normal breast tissue and assumed a cytoplasmic distribution. In contrast, CAPER was expressed at higher levels in ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) specimens, where it assumed a predominantly nuclear distribution. However, the functional role of CAPER in human breast cancer initiation and progression remained unknown. Here, we used a lentiviral-mediated gene silencing approach to reduce the expression of CAPER in the ER-positive human breast cancer cell line MCF-7. The proliferation and tumorigenicity of MCF-7 cells stably expressing control or human CAPER shRNAs was then determined via both in vitro and in vivo experiments. Knockdown of CAPER expression significantly reduced the proliferation of MCF-7 cells in vitro. Importantly, nude mice injected with MCF-7 cells harboring CAPER shRNAs developed smaller tumors than mice injected with MCF-7 cells harboring control shRNAs. Mechanistically, tumors derived from mice injected with MCF-7 cells harboring CAPER shRNAs displayed reduced expression of the cell cycle regulators PCNA, MCM7, and cyclin D1, and the protein synthesis marker 4EBP1. In conclusion, knockdown of CAPER expression markedly reduced human breast cancer cell proliferation in both in vitro and in vivo settings. Mechanistically, knockdown of CAPER abrogated the activity of proliferative and protein synthesis pathways.
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