miR-485-5p suppresses breast cancer progression and chemosensitivity by targeting survivin

Wang, Meng; Cai, Wenbin; Meng, Ran; Jiang, Rui; Li, Yun Rui; Chen, Ao Xiang; Yu, Yue; Cao, Xuchen

doi:10.1016/j.bbrc.2018.04.129

Cited by 50 publications

(37 citation statements)

References 25 publications

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“…This clearly underlines the cell type-specific effect of miRNAs despite the nature of the disease. Although miR-485-5p has been shown to suppress breast cancer and hepatocellular carcinoma progression [ 44 , 45 ], the proliferation of NSCLC [46] , its reduced expression was associated with poor gastric cancer prognosis [47] . Such a complexity indicate that the stage-specific effects of Akt on PCa growth and metastasis is orchestrated by several but not a single miRNA.…”

Section: Discussionmentioning

confidence: 99%

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Alwhaibi

Gao

Artham

et al. 2018

Heliyon

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Recent studies indicate a stage-specific, differential role for the oncogene Akt on various cancers. In prostate cancer (PCa), suppression of Akt activity in the advanced stages promoted transforming growth factor-β (TGFβ) pathway-mediated epithelial-to-mesenchymal transition (EMT) and metastasis to the lungs. In the current study, we performed Affymetrix analysis to compare the expression profile of microRNAs in the mouse prostate tissues collected at the prostatic inter-epithelial neoplasia (PIN) stage from Transgenic adenocarcinoma of the mouse (TRAMP)/Akt1+/+ versus TRAMP/Akt1–/– mice, and at the advanced stage from TRAMP/Akt1+/+ mice treated with triciribine (Akt inhibitor) versus DMSO-treated control. Our analysis demonstrates that in the early stage, Akt1 in the TRAMP prostate tumors express a set of miRNAs responsible for regulating cancer cell survival, proliferation, and tumor growth, whereas, in the advanced stages, a different set of miRNAs that promote EMT and cancer metastasis is expressed. Our study has identified novel Akt-regulated signature microRNAs in the early and advanced PCa and demonstrates their differential effects on PCa growth and metastasis.

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Section: Discussionmentioning

confidence: 99%

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Alwhaibi

Gao

Artham

et al. 2018

Heliyon

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“…Nevertheless, a breakthrough to find survivin mRNA inhibitors may come from the siRNA approach in combination with the development of nanotechnology for delivery [119][120][121][122][123][124][125][126][127][128][129][130][131], since survivin siRNA design in the coming years might take inspiration from various miRNA-mediated survivin mRNA inhibition. Currently miRNA regulation of survivin mRNA/transcripts is a hot research area, which has room for further in depth, extended studies (see Table 1) [146][147][148][149]. The current status of study in this area is that, while many miRNAs were found to bind to survivin mRNA/transcripts with defined inhibitory effects, many other miRNAs were found to bind to survivin transcripts/mRNAs without defined effects (Table 1), which calls for further investigation.…”

Section: Spc3042/ezn-3042mentioning

confidence: 99%

Cancer therapeutics using survivin BIRC5 as a target: what can we do after over two decades of study?

Aljahdali

Ling

2019

J Exp Clin Cancer Res

177

161

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Survivin (also named BIRC5) is a well-known cancer therapeutic target. Since its discovery more than two decades ago, the use of survivin as a target for cancer therapeutics has remained a central goal of survivin studies in the cancer field. Many studies have provided intriguing insight into survivin's functional role in cancers, thus providing promise for survivin as a cancer therapeutic target. Despite this, moving survivin-targeting agents into and through the clinic remains a challenge. In order to address this challenge, we may need to rethink current strategies in order to develop a new mindset for targeting survivin. In this Review, we will first summarize the current survivin mechanistic studies, and then review the status of survivin cancer therapeutics, which is classified into five categories: (i) survivin-partner protein interaction inhibitors, (ii) survivin homodimerization inhibitors, (iii) survivin gene transcription inhibitors, (iv) survivin mRNA inhibitors and (v) survivin immunotherapy. We will then provide our opinions on cancer therapeutics using survivin as a target, with the goal of stimulating discussion that might facilitate translational research for discovering improved strategies and/or more effective anticancer agents that target survivin for cancer therapy.

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“…Cells were seeded in 24-well plates and collected 48 h after transfection. The luciferase activity was determined by a Dual-Luciferase Reporter Assay System (Promega) according to the manufacturer's recommendations, as previously described 34 . All transfections were performed in triplicate.…”

Section: Luciferase Reporter Assaymentioning

confidence: 99%

LINC00665 promotes breast cancer progression through regulation of the miR-379-5p/LIN28B axis

Diao

Qiu

et al. 2020

Cell Death Dis

Self Cite

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Breast cancer is the most common malignant tumor among women worldwide. Although increasing evidence indicates that long noncoding RNAs (lncRNAs) play critical roles during breast tumorigenesis and progression, the involvement of most lncRNAs in breast cancer remains largely unknown. In the current study, we demonstrated that LINC00665 promotes breast cancer cell proliferation, migration, and invasion. Accumulating evidence indicates that many lncRNAs can function as endogenous miRNA sponges by competitively binding common miRNAs. In this study, we demonstrated that LINC00665 functions as a sponge for miR-379-5p, reducing the ability of miR-379-5p to repress LIN28B. LINC00665 promoted breast cancer progression and induced an epithelial-mesenchymal transition-like phenotype via the upregulation of LIN28B expression. Clinically, LINC00665 expression was increased but miR-379-5p expression was decreased in breast cancer tissues compared with that in normal breast tissues in the TCGA database. Furthermore, the expression of LINC00665 was negatively related with miR-379-5p expression. Collectively, our results reveal the LINC00665-miR-379-5p-LIN28B axis and shed light on breast cancer therapy.

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miR-485-5p suppresses breast cancer progression and chemosensitivity by targeting survivin

Cited by 50 publications

References 25 publications

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Cancer therapeutics using survivin BIRC5 as a target: what can we do after over two decades of study?

LINC00665 promotes breast cancer progression through regulation of the miR-379-5p/LIN28B axis

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