The synergy between miR-486–5p and tamoxifen causes profound cell death of tamoxifen-resistant breast cancer cells

Mansoori, Behzad; Najafi, Souzan; Mohammadi, Ali; AsadollahSeraj, Haleh; Savadi, Pouria; Mansoori, Behnaz; Nazari, Afsaneh; Mokhtarzadeh, Ahad; Roshani, Elmira; Duijf, Pascal H.G.; Cho, William C.; Baradaran, Behzad

doi:10.1016/j.biopha.2021.111925

Cited by 12 publications

(6 citation statements)

References 35 publications

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“…[45] Aiming at the generally believes that miR-486-5p is a tumor suppressor gene. [46][47][48] Studies have shown that miR-486-5p can enhance cisplatin sensitivity of bladder cancer cells. [49,50] Notably, the molecular and cellular mechanisms of cisplatin-induced nephrotoxicity are crucially involved in the cytotoxic activity of cisplatin against tumor cells and potential alterations in their function might mitigate cisplatin-induced antitumor effects.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐486‐5p is implicated in the cisplatin‐induced apoptosis and acute inflammation response of renal tubular epithelial cells by targeting HAT1

Lin

Han

et al. 2022

J Biochem & Molecular Tox

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The proinflammatory property of cisplatin is potentially destructive and contributes to the pathogenesis of acute kidney injury (AKI). The role and upstream regulatory mechanism of histone acetyltransferase 1 (HAT1) in acute kidney inflammation are still unknown. We performed RNA sequencing to filter differentially expressed microRNAs (miRNAs) in the kidney tissue of mice with AKI induced by cisplatin and ischemia-reperfusion. Here, we found that miR-486-5p was upregulated and that the expression of HAT1 was reduced in AKI mouse models and injured human renal proximal tubular epithelial cell (HK-2) model induced by cisplatin. miR-486-5p is implicated in cisplatin-induced kidney damage in vivo. Bioinformatics analysis predicted a potential binding site between miR-486-5p and HAT1. The Luciferase reporter assay and Western blot confirmed that miR-486-5p directly targeted the 3′-untranslated region of HAT1 mRNA and inhibited its expression in the cytoplasm of HK-2 cells. In the in vitro study, inhibiting miR-486-5p reduced apoptosis, and the expression of proinflammatory mediators was induced by cisplatin in HK-2 cells.Simultaneously, the downregulation of miR-486-5p inhibited the activation of the toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB). We further found that HAT1 could inhibit apoptosis and the activation of cisplatin on the TLR4/NF-κB pathway and that the upregulation of miR-486-5p reversed this effect. Therefore, the upregulation of miR-486-5p targeting HAT1 promoted the cisplatin-induced apoptosis and acute inflammation response of renal tubular epithelial cells by activating the TLR4/NF-κB pathway, providing a new basis to highlight the potential intervention of regulating the miR-486-5p/HAT1 axis.

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Section: Discussionmentioning

confidence: 99%

microRNA‐486‐5p is implicated in the cisplatin‐induced apoptosis and acute inflammation response of renal tubular epithelial cells by targeting HAT1

Lin

Han

et al. 2022

J Biochem & Molecular Tox

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“…We demonstrated that downregulation of hsa-mir-486-5p was significantly associated with PTC progression. Several studies have demonstrated the role of hsa-mir-486-5p in numerous human cancers ( 53 – 57 ). For instance, mir-486-5p was markedly downregulated in non-small cell lung cancer (NSCLS), gastric cancer, hepatocellular carcinoma, and colorectal and pancreatic cancer ( 53 , 54 , 58 – 60 ).…”

Section: Discussionmentioning

confidence: 99%

Construction of a Signature Model to Predict the Radioactive Iodine Response of Papillary Thyroid Cancer

et al. 2022

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Papillary thyroid cancer (PTC) accounts for about 90% of thyroid cancer. There are approximately 20%–30% of PTC patients showing disease persistence/recurrence and resistance to radioactive iodine (RAI) treatment. For these PTC patients with RAI refractoriness, the prognosis is poor. In this study, we aimed to establish a comprehensive prognostic model covering multiple signatures to increase the predictive accuracy for progression-free survival (PFS) of PTC patients with RAI treatment. The expression profiles of mRNAs and miRNAs as well as the clinical information of PTC patients were extracted from TCGA and GEO databases. A series of bioinformatics methods were successfully applied to filtrate a two-RNA model (IPCEF1 and hsa-mir-486-5p) associated with the prognosis of RAI-therapy. Finally, the RNA-based risk score was calculated based on the Cox coefficient of the individual RNA, which achieved good performances by the time-dependent receiver operating characteristic (tROC) curve and PFS analyses. Furthermore, the predictive power of the nomogram, integrated with the risk score and clinical parameters (age at diagnosis and tumor stage), was assessed by tROC curves. Collectively, our study demonstrated high precision in predicting the RAI response of PTC patients.

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“…For example, let-7 is one of the earliest discovered microRNAs. Let-7a, a member of its family, can significantly downregulate the target gene HMGA1 to affect growth 49 ; miR-142-3p and miR-26a can be used as tumour suppressors to inhibit the expression of oncogene HMGA1 50 , 51 ; miR-661 induces apoptosis after downregulating HMGA1 52 ; and miR-486-5p leads to G2/M cell cycle arrest and profound cell death of breast cancer cells by downregulating HMGA1 53 . LINC00963 competes with miR-625 for endogenous RNA and attenuated the inhibitory effect of miR-625 on HMGA1 54 .…”

Section: The Role Of Hmga1 In Cancermentioning

confidence: 99%

High Mobility Group A1 (HMGA1): Structure, Biological Function, and Therapeutic Potential

Wang¹,

Zhang²,

Xia³

et al. 2022

Int. J. Biol. Sci.

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High mobility group A1 (HMGA1) is a nonhistone chromatin structural protein characterized by no transcriptional activity. It mainly plays a regulatory role by modifying the structure of DNA. A large number of studies have confirmed that HMGA1 regulates genes related to tumours in the reproductive system, digestive system, urinary system and haematopoietic system. HMGA1 is rare in adult cells and increases in highly proliferative cells such as embryos. After being stimulated by external factors, it will produce effects through the Wnt/β-catenin, PI3K/Akt, Hippo and MEK/ERK pathways. In addition, HMGA1 also affects the ageing, apoptosis, autophagy and chemotherapy resistance of cancer cells, which are linked to tumorigenesis. In this review, we summarize the mechanisms of HMGA1 in cancer progression and discuss the potential clinical application of targeted HMGA1 therapy, indicating that targeted HMGA1 is of great significance in the diagnosis and treatment of malignancy.

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The synergy between miR-486–5p and tamoxifen causes profound cell death of tamoxifen-resistant breast cancer cells

Cited by 12 publications

References 35 publications

microRNA‐486‐5p is implicated in the cisplatin‐induced apoptosis and acute inflammation response of renal tubular epithelial cells by targeting HAT1

microRNA‐486‐5p is implicated in the cisplatin‐induced apoptosis and acute inflammation response of renal tubular epithelial cells by targeting HAT1

Construction of a Signature Model to Predict the Radioactive Iodine Response of Papillary Thyroid Cancer

High Mobility Group A1 (HMGA1): Structure, Biological Function, and Therapeutic Potential

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