ArticleCancer letters2018
Survivin-targeting miR-542-3p overcomes HER3 signaling-induced chemoresistance and enhances the antitumor activity of paclitaxel against HER2-overexpressing breast cancer.
Article in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- miR-542-3p targets TTF1 to regulate proliferation, invasion, and migration of lung adenocarcinoma via the MAPK signaling pathway.Scientific reports · 2026Article
- Article
- HER3 promotes triple-negative breast cancer progression by upregulating PHF8 via miR-34b-5p-dependent mechanism.Cell death & disease · 2025Article
- MicroRNA dynamics, PTEN/PI3K/AKT signaling, and their relationship to breast cancer: prospects for pharmaceuticals and natural product application.Breast cancer research and treatment · 2025Review
- miR-328-3p suppresses hepatocellular carcinoma progression by regulating HMOX1 expression.Discover oncology · 2024Article
- HER3 functions as an effective therapeutic target in triple negative breast cancer to potentiate the antitumor activity of gefitinib and paclitaxel.Cancer cell international · 2023Article
- HER3 targeting augments the efficacy of panobinostat in claudin-low triple-negative breast cancer cells.NPJ precision oncology · 2023Article
- Trastuzumab-resistant breast cancer cells-derived tumor xenograft models exhibit distinct sensitivity to lapatinib treatment in vivo.Biological procedures online · 2023Article
- Molecular mechanisms of resveratrol as chemo and radiosensitizer in cancer.Frontiers in pharmacology · 2023Review
- CircRBM33 downregulation inhibits hypoxia-induced glycolysis and promotes apoptosis of breast cancer cells via a microRNA-542-3p/HIF-1α axis.Cell death discovery · 2022Article
- circ_PTN contributes to -cisplatin resistance in glioblastoma via PI3K/AKT signaling through the miR-542-3p/PIK3R3 pathway.Molecular therapy. Nucleic acids · 2021Article
- Upregulation of endogenous TRAIL-elicited apoptosis is essential for metformin-mediated antitumor activity against TNBC and NSCLC.Molecular therapy oncolytics · 2021Article
- Micro-RNA miR-542-3p suppresses decidualization by targeting ILK pathways in human endometrial stromal cells.Scientific reports · 2021Article
- Hsa-miR-5581-3p and Hsa-miR-542-3p Target theMediterranean journal of hematology and infectious diseases · 2021Article
- MicroRNAs: Important Players in Breast Cancer Angiogenesis and Therapeutic Targets.Frontiers in molecular biosciences · 2021Review
- Targeting the Human Epidermal Growth Factor Receptor Family in Breast Cancer beyond HER2.Breast care (Basel, Switzerland) · 2020Review
- Participation of MicroRNAs in the Treatment of Cancer with Phytochemicals.Molecules (Basel, Switzerland) · 2020Review
- Identification of an independent autophagy-gene prognostic index for papillary renal cell carcinoma.Translational andrology and urology · 2020Article
- Connecting the Missing Dots: ncRNAs as Critical Regulators of Therapeutic Susceptibility in Breast Cancer.Cancers · 2020Review
- Enhanced Cellular Uptake and Gene Silencing Activity of Survivin-siRNA via Ultrasound-Mediated Nanobubbles in Lung Cancer Cells.Pharmaceutical research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Elevated expression of HER3, which interacts with HER2 in breast cancer cells, confers chemoresistance via phosphoinositide 3-kinase (PI-3K)/Akt-dependent upregulation of Survivin. However, the underlying mechanism is not clear. Ectopic expression or specific knockdown of HER3 in HER2-overexpressing breast cancer cells did not alter Survivin mRNA levels and Survivin protein stability, supporting the notion that HER3 signaling may regulate specific miRNAs that target Survivin to alter its protein translation. Here we showed that overexpression and specific knockdown of HER3 reduced and enhanced expression of two Survivin-targeting miRNAs, miR-203 and miR-542-3p, in breast cancer cells, respectively. While the specific inhibitor of either miR-203 or miR-542-3p attenuated an anti-HER3 antibody-induced downregulation of Survivin, inhibition of miR-542-3p exhibited a better efficacy than miR-203 inhibition did. Consistently, miR-542-3p mimic was much more effective than miR-203 mimic not only in inhibition of Survivin, but also in enhancement of paclitaxel-induced apoptosis in HER2-overexpressing breast cancer cells. Moreover, the combination of miR-542-3p mimic and paclitaxel, as compared with either agent alone, significantly inhibited in vivo tumor growth of HER2-overexpressing breast cancer cells. Collectively, our data indicated that the HER3/PI-3K/Akt signaling upregulates Survivin via suppression of miR-203 and miR-542-3p. Because miR-542-3p has three binding sites on the 3'-UTR of Survivin mRNA, its mimic was able to effectively downregulate Survivin in vitro and in vivo. Thus, miR-542-3p-replacement therapy is an excellent approach to overcome HER3-mediated paclitaxel resistance and significantly enhances the antitumor activity of paclitaxel against HER2-overexpressing breast cancer.
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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 OpenQuestion graph.