<i>Retracted</i>: Downregulation of microRNA‐1469 promotes the development of breast cancer via targeting HOXA1 and activating PTEN/PI3K/AKT and Wnt/β‐catenin pathways

Zhang, Yonghui; Fang, Jing; Zhao, Hongmeng; Yu, Yue; Cao, Xuchen; Zhang, Bin

doi:10.1002/jcb.27786

Cited by 16 publications

(6 citation statements)

References 31 publications

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“…cancers. Consistently, low expression levels of microRNAs targeting HOXA1 are also associated with poor prognosis and Tamoxifen resistance (3,(62)(63)(64)(65)(66). Therefore, early de novo HOXA1 expression in the mammary gland might lead to the development of aggressive subtypes of breast cancer, and late HOXA1 expression in an ER+ tumor environment might lead to endocrine therapy resistance.…”

Section: Discussionmentioning

confidence: 98%

HOXA1 Is an Antagonist of ERα in Breast Cancer

et al. 2021

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Breast cancer is a heterogeneous disease and the leading cause of female cancer mortality worldwide. About 70% of breast cancers express ERα. HOX proteins are master regulators of embryo development which have emerged as being important players in oncogenesis. HOXA1 is one of them. Here, we present bioinformatic analyses of genome-wide mRNA expression profiles available in large public datasets of human breast cancer samples. We reveal an extremely strong opposite correlation between HOXA1 versus ER expression and that of 2,486 genes, thereby supporting a functional antagonism between HOXA1 and ERα. We also demonstrate in vitro that HOXA1 can inhibit ERα activity. This inhibition is at least bimodal, requiring an intact HOXA1 DNA-binding homeodomain and involving the DNA-binding independent capacity of HOXA1 to activate NF-κB. We provide evidence that the HOXA1-PBX interaction known to be critical for the transcriptional activity of HOXA1 is not involved in the ERα inhibition. Finally, we reveal that HOXA1 and ERα can physically interact but that this interaction is not essential for the HOXA1-mediated inhibition of ERα. Like other HOX oncoproteins interacting with ERα, HOXA1 could be involved in endocrine therapy resistance.

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Section: Discussionmentioning

confidence: 98%

HOXA1 Is an Antagonist of ERα in Breast Cancer

et al. 2021

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“…Firstly, we tested HOXA1 and verified it as a direct target of miR-10b. As one of the HOX family members, HOXA1 is involved in various biological processes, including cell apoptosis and growth (Zhang et al, 2018). For instance, it was demonstrated that HOXA1 can inhibit the migration, invasion and growth of HepG2 cells (Zha et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Bta-miR-10b Secreted by Bovine Embryos Negatively Impacts Preimplantation Embryo Quality

et al. 2019

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In a previous study, we found miR-10b to be more abundant in a conditioned culture medium of degenerate embryos compared to that of blastocysts. Here, we show that miR-10b mimics added to the culture medium can be taken up by embryos. This uptake results in an increase in embryonic cell apoptosis and aberrant expression of DNA methyltransferases ( DNMTs ). Using several algorithms, Homeobox A1 ( HOXA1 ) was identified as one of the potential miR-10b target genes and dual-luciferase assay confirmed HOXA1 as a direct target of miR-10b. Microinjection of si- HOXA1 into embryos also resulted in an increase in embryonic cell apoptosis and downregulation of DNMTs . Cell progression analysis using Madin–Darby bovine kidney cells (MDBKs) showed that miR-10b overexpression and HOXA1 knockdown results in suppressed cell cycle progression and decreased cell viability. Overall, this work demonstrates that miR-10b negatively influences embryo quality and might do this through targeting HOXA1 and/or influencing DNA methylation.

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“…Studies have found that p53 can up-regulate the expression of miR-29c in colon carcinoma cells, and miR-29c can act on its downstream target gene PHLDB2 to down-regulate its expression, thereby inhibiting the invasion and metastasis of colon carcinoma cells. By contrast, the binding site of p53 and miR-17-92 promoter region covers the TATA box region, thus interfering with the binding of TATA box binding protein (TBP) with TATA box, thereby inhibiting the transcription of miR-17-92 and down-regulating its expression level (Zhang et al, 2018a;Zhang et al, 2018b;Zhang et al,2018c).…”

Section: Discussionmentioning

confidence: 99%

Study on Forsythin promoting apoptosis of laryngeal carcinoma cells by regulating miRNA-1469

et al. 2022

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Objective: The paper aimed to explore the mechanism of Forsythin regulating miRNA expression in laryngeal carcinoma cells, and to clarify the molecular biological mechanism of Forsythin regulating miRNA to promote the apoptosis of laryngeal carcinoma cells, providing theoretical and experimental basis for clinical application of Forsythin as an anti-laryngeal cancer treatment drug. Methods: A miR-1469 low-expression laryngeal carcinoma cell line was established. Western blot and flow cytometry were applied to detect the effect of Forsythin on cell apoptosis. Western blot was employed to detect the effects of Forsythin on P53 protein, P53 low expression, and P53 overexpression in laryngeal carcinoma cells, as well as the effects on overexpression of miRNA-1469, and on double low expression of P53 and Mcl1. Real-time PCR method was used to detect the effect of miR-1469 on p53 low expression in laryngeal carcinoma cells. Results: Flow cytometry detection of cell apoptosis showed that, after the cells with low miR-1469 expression were treated with Forsythin, the apoptosis rate was significantly reduced. Western blot detection showed that, compared with the Control group, the expression level of miR-1469 was significantly reduced after Forsythin administration in Hep2 cells with low expression of P53. Compared with the idle Control group, the apoptosis level of laryngeal carcinoma cells in Hep2 cells with low expression of P53 was significantly reduced. In Hep2 cells transfected with P53 overexpression plasmids, apoptosis level of laryngeal carcinoma cells increased. Compared with the idle Control group, the apoptosis level of laryngeal carcinoma cells in the single-transformed P53 shRNA group decreased, while the apoptosis level of the double-transformed miR-1469 mimic+P53 shRNA group increased again. After drug treatment, the apoptosis level of the single-transformed P53 shRNA group decreased, while the apoptosis level of the double-transformed Mcl1 shRNA+P53 shRNA group increased again. Conclusion: Forsythin can promote the apoptosis of laryngeal carcinoma cells by up-regulating the expression of miR-1469 and then down-regulating the expression of Mcl1. The drug can up-regulate the expression of miR-1469 by elevating the expression of P53. miR-1469 can promote the apoptosis of laryngeal carcinoma cells by inhibiting the expression of its downstream target gene Mcl1.

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Retracted: Downregulation of microRNA‐1469 promotes the development of breast cancer via targeting HOXA1 and activating PTEN/PI3K/AKT and Wnt/β‐catenin pathways

Cited by 16 publications

References 31 publications

HOXA1 Is an Antagonist of ERα in Breast Cancer

HOXA1 Is an Antagonist of ERα in Breast Cancer

Bta-miR-10b Secreted by Bovine Embryos Negatively Impacts Preimplantation Embryo Quality

Study on Forsythin promoting apoptosis of laryngeal carcinoma cells by regulating miRNA-1469

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