ArticleAmerican journal of cancer research2019
Prolactin-inducible EDD E3 ubiquitin ligase promotes TORC1 signalling, anti-apoptotic protein expression, and drug resistance in breast cancer cells.
Article in American journal of cancer research, 2019. 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, 17 citations in OpenAlex.
- Review
- SF3A2 promotes progression and cisplatin resistance in triple-negative breast cancer via alternative splicing of MKRN1.Science advances · 2024Article
- The crosstalk between ubiquitination and endocrine therapy.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Hormone supply to the pituitary gland: A comprehensive investigation of female‑related tumors (Review).International journal of molecular medicine · 2022Review
- Diallyl disulfide and diallyl trisulfide in garlic as novel therapeutic agents to overcome drug resistance in breast cancer.Journal of pharmaceutical analysis · 2022Review
- Prolactin receptor signaling: A novel target for cancer treatment - Exploring anti-PRLR signaling strategies.Frontiers in endocrinology · 2022Review
- Article
- The Relevant Participation of Prolactin in the Genesis and Progression of Gynecological Cancers.Frontiers in endocrinology · 2021Review
- Prolactin and androgen R1881 induce pro-survival carboxypeptidase-D and EDD E3 ligase in triple-negative and HER2+ breast cancer.American journal of cancer research · 2020Article
- Loss ofFrontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, we identified a prolactin (PRL)-inducible gene encoding EDD E3 ubiquitin ligase in human breast cancer (BCa) cells. We reported that EDD binds the mTOR (TORC1)-associated α4 phosphoprotein-PP2Ac protein phosphatase complex that regulates initiation of translation and cell cycle progression, and that EDD targets PP2Ac for proteasomal degradation. The present study showed that EDD immunostaining was low in benign human breast tissues, but increased progressively in ductal carcinoma in-situ, low-grade, and high-grade BCa, and in triple-negative BCa (TNBC). EDD mRNA and protein levels varied in human BCa cell lines. In high-EDD expressing MCF-7 and T47D cells, siRNA knockdown of EDD arrested cells in the G2-phase of the cell cycle, decreased cell viability, and increased apoptosis. EDD siRNA-induced apoptosis in MCF-7 cells correlated with significantly increased levels of pro-apoptotic Bim and Bak mRNAs and proteins (P < 0.05, n = 3-6), and increased levels of pro-apoptotic Bax and MOAP-1 proteins (P < 0.001, n = 3-6), leading to increased cleavage of caspase-7 and caspase substrate poly-ADP-ribose polymerase-1 (PARP-1), as compared to control cells. Loss of EDD in MCF-7 cells decreased PRL-induced phosphorylation of eukaryotic initiation factor 4E-binding protein-1, a mediator of TORC1 signaling, resulting in decreased binding of 4E to γ-aminophenyl-m
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Identifiers
31392083PMC6682715W2986966971What OpenQuestion holds
Registered trials
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