MicroRNA-29a contributes to drug-resistance of breast cancer cells to adriamycin through PTEN/AKT/GSK3β signaling pathway

Shen, Huan; Li, Liangpeng; Yang, Su-Jin; Wang, Dandan; Zhong, Shanliang; Zhao, Jinmin; Tang, Jinhai

doi:10.1016/j.gene.2016.08.016

Cited by 73 publications

(53 citation statements)

References 27 publications

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“…In this study, our data revealed the essential role of PTEN in the regulation of the Akt/GSK-3b/ b-catenin pathway following ethanol treatment. Other studies have demonstrated similar results: the PTEN/ AKT/GSK-3b pathway plays an important role in the regulation of cell proliferation and differentiation [43,44]. In addition, mammalian target of rapamycin (mTOR), one of the essential downstream targets of PI3K/AKT signaling, is a regulator of cell proliferation and differentiation [45,46].…”

Section: Discussionmentioning

confidence: 63%

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

et al. 2019

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Alcohol is considered a leading risk factor for osteopenia. Our previous research indicated that the Akt/GSK‐3β/β‐catenin pathway plays a critical role in the ethanol‐induced antiosteogenic effect in bone mesenchymal stem cells (BMSCs). PI3K/Akt is negatively regulated by the phosphatase and tensin homolog (PTEN) phosphatase. In this study, we found that ethanol increased PTEN expression in the BMSCs and bone tissue of ethanol‐treated Sprague–Dawley rats. PTEN upregulation impaired Akt recruitment to the plasma membrane and suppressed Akt phosphorylation at Ser473, thereby inhibiting Akt/GSK3β/β‐catenin signaling and the expression of COL1 and OCN in BMSCs in vitro and in vivo. The results of in vivo assays indicated that PTEN inhibition protected bone tissue against ethanol. Interestingly, our data revealed that following ethanol stimulation, PTEN and PTEN pseudogene 1 (PTENP1) mRNA expression was increased in a time‐dependent manner, resulting in an increased PTEN protein level. In addition, ethanol upregulated PTEN expression and decreased PTEN phosphorylation (p‐PTEN), indicating an increase in functional PTEN levels. In summary, the ethanol‐mediated transcriptional and post‐transcriptional regulation of PTEN impaired downstream Akt/GSK3β/β‐catenin signaling and BMSC osteogenic differentiation. Therefore, we propose that Akt/GSK3β/β‐catenin activation via PTEN inhibition may be a potential therapeutic approach for preventing the development of alcohol‐induced osteopenia.

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Section: Discussionmentioning

confidence: 63%

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

et al. 2019

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“…For example, they can contribute in BC to the acquisition of doxorubicin resistance by inhibition of PTEN/AKT/GSK3β (241). Conversely, miR-29b exerts a tumor suppressor activity in tamoxifen-resistant BC cells (242).…”

Section: A Network Analysis: the Most Central Ncrnas In Chemoresistancementioning

confidence: 99%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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Non-coding RNAs (ncRNAs) have been implicated in most cellular functions. The disruption of their function through somatic mutations, genomic imprinting, transcriptional and post-transcriptional regulation, plays an ever-increasing role in cancer development. ncRNAs, including notorious microRNAs, have been thus proposed to function as tumor suppressors or oncogenes, often in a context-dependent fashion. In parallel, ncRNAs with altered expression in cancer have been reported to exert a key role in determining drug sensitivity or restoring drug responsiveness in resistant cells. Acquisition of resistance to anti-cancer drugs is a major hindrance to effective chemotherapy and is one of the most important causes of relapse and mortality in cancer patients. For these reasons, non-coding RNAs have become recent focuses as prognostic agents and modifiers of chemo-sensitivity. This review starts with a brief outline of the role of most studied non-coding RNAs in cancer and then highlights the modulation of cancer drug resistance via known ncRNAs based mechanisms. We identified from literature 388 ncRNA-drugs interactions and analyzed them using an unsupervised approach. Essentially, we performed a network analysis of the non-coding RNAs with direct relations with cancer drugs. Within such a machine-learning framework we detected the most representative ncRNAs-drug associations and groups. We finally discussed the higher integration of the drug-ncRNA clusters with the goal of disentangling effectors from downstream effects and further clarify the involvement of ncRNAs in the cellular mechanisms underlying resistance to cancer treatments.

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“…The study conducted by Shen and colleagues recognized the effect of up-regulated miR-29a-3p in exacerbating doxorubicin-resistance in breast cancer cell lines, through its regulatory function on PTEN and GSK3β, that are two major components of the PTEN/AKT/GSK3β signalling pathway providing feedback to TP53 [55]. Further evidence for such miRNA influences on p53 modulation include the study carried out by Qin and colleagues, who revealed that the over-expression of miR-182-5p can induce cisplatin chemoresistance in hepatocellular carcinoma HepG2-Rcells [130].…”

Section: Influences Of Mirnas In Cancer Chemoresistancementioning

confidence: 99%

Influence of microRNAs and Long Non-Coding RNAs in Cancer Chemoresistance

Ayers

Vandesompele

2017

Genes

100

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Innate and acquired chemoresistance exhibited by most tumours exposed to conventional chemotherapeutic agents account for the majority of relapse cases in cancer patients. Such chemoresistance phenotypes are of a multi-factorial nature from multiple key molecular players. The discovery of the RNA interference pathway in 1998 and the widespread gene regulatory influences exerted by microRNAs (miRNAs) and other non-coding RNAs have certainly expanded the level of intricacy present for the development of any single physiological phenotype, including cancer chemoresistance. This review article focuses on the latest research efforts in identifying and validating specific key molecular players from the two main families of non-coding RNAs, namely miRNAs and long non-coding RNAs (lncRNAs), having direct or indirect influences in the development of cancer drug resistance properties and how such knowledge can be utilised for novel theranostics in oncology.

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MicroRNA-29a contributes to drug-resistance of breast cancer cells to adriamycin through PTEN/AKT/GSK3β signaling pathway

Cited by 73 publications

References 27 publications

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

The Network of Non-coding RNAs in Cancer Drug Resistance

Influence of microRNAs and Long Non-Coding RNAs in Cancer Chemoresistance

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