MicroRNA-100 promotes migration and invasion through mammalian target of rapamycin in esophageal squamous cell carcinoma

Zhang, Naijian; Fu, Hailong; Song, Lixia; Ding, Youhong; XiuFang, Wang; Zhao, Cheng; Zhao, Yiqi; Jiao, Feng; Zhao, Yaping

doi:10.3892/or.2014.3389

Cited by 22 publications

(14 citation statements)

References 39 publications

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“…The dual findings that miR-100 is also carried by MSC- and HSC-derived EVs [27], and that miR-100 post-transcriptionally regulates mTOR [37], led us to investigate whether it can also contribute to EV-mediated effects. First, miR-100 expression was evaluated in MCs subjected to EV treatment.…”

Section: Resultsmentioning

confidence: 99%

“…EVs have also been shown to display a therapeutic effect via the transfer of various miRs with protective activity [22,23,27,30]. Other potential therapeutic miRs were identified by investigating MSC and HLSC EV content, including miR-100 [27], which has been shown to target mTOR [37]. Although miR-100 content increases in HG-treated MC cells, possibly as a protective mechanism, its expression did not change upon EV treatment.…”

Section: Discussionmentioning

confidence: 99%

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Stem Cell-Derived, microRNA-Carrying Extracellular Vesicles: A Novel Approach to Interfering with Mesangial Cell Collagen Production in a Hyperglycaemic Setting

et al. 2016

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Extracellular vesicles (EVs) that are derived from stem cells are proving to be promising therapeutic options. We herein investigate the therapeutic potential of EVs that have been derived from different stem cell sources, bone-marrow (MSC) and human liver (HLSC), on mesangial cells (MCs) exposed to hyperglycaemia. By expressing a dominant negative STAT5 construct (ΔNSTAT5) in HG-cultured MCs, we have demonstrated that miR-21 expression is under the control of STAT5, which translates into Transforming Growth Factor beta (TGFβ) expression and collagen production. A number of approaches have been used to show that both MSC- and HLSC-derived EVs protect MCs from HG-induced damage via the transfer of miR-222. This resulted in STAT5 down-regulation and a decrease in miR-21 content, TGFβ expression and matrix protein synthesis within MCs. Moreover, we demonstrate that changes in the balance between miR-21 and miR-100 in the recipient cell, which are caused by the transfer of EV cargo, further contribute to providing beneficial effects. Interestingly, these effects were only detected in HG-cultured cells. Finally, it was found that HG reduced the expression of the nuclear encoded mitochondrial electron transport chain (ETC) components, CoxIV. It is worth noting that EV administration can rescue CoxIV expression in HG-cultured MCs. These results thus demonstrate that both MSC- and HLSC-derived EVs transfer the machinery needed to preserve MCs from HG-mediated damage. This occurs via the horizontal transfer of functional miR-222 which directly interferes with damaging cues. Moreover, our data indicate that the release of EV cargo into recipient cells provides additional therapeutic advantages against harmful mitochondrial signals.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Stem Cell-Derived, microRNA-Carrying Extracellular Vesicles: A Novel Approach to Interfering with Mesangial Cell Collagen Production in a Hyperglycaemic Setting

et al. 2016

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“…Recently, the lower expression of miR-100 in bladder cancer tissues compared to adjacent noncancerous tissues is reported to be correlated with low-grade, non-invasive bladder urothelial cancer [50,52,54]. In ESCC, miR-100 demonstrated markedly lower expression in tumor tissues than in controls as validated by quantitative reverse transcription-polymerase chain reaction [30]. Feng et al found that the expression of miR-100 in docetaxel-resistant lung adenocarcinoma cell line (SPC-A1/DTX) is significantly lower than that in parental SPC-A1 cells [35].…”

Section: Mir-100 In Cancer Diagnosis and Prognosismentioning

confidence: 99%

“…Bhushan et al showed that miR-100 in breast cancer could target the kinasedeficient EphB6 receptor to initiate signal transduction from the cell surface to the nucleus and alter tumorigenesis and invasion [96]. Moreover, Zhang et al demonstrated that miR-100 modulated the migration and invasion of ESCC cells by targeting the mTOR 3'-UTR, and its downregulation in ESCC tissues was significantly correlated with status of lymph node metastasis in patients [30]. Argonaute 2 (AGO2), the core effector protein of the miRNAinduced silencing complex promotes tumor metastasis.…”

Section: Mir-100 In Cancer Invasion and Metastasismentioning

confidence: 99%

Multiple Roles of MicroRNA-100 in Human Cancer and its Therapeutic Potential

Li¹,

Gao²,

Zhang³

et al. 2015

Cell Physiol Biochem

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MicroRNAs (miRNAs) are a recently discovered class of endogenous, small (about 22 nucleotides) non-coding RNAs, which play important roles in cancer development and progression. Emerging evidence shows that microRNAs exert their regulatory effects by directly binding to the 3'- untranslated regions (UTRs) of their target genes. MicroRNA-100 (miR-100) is aberrantly expressed and functions in many human cancers by regulating multiple cell processes, such as cell cycle, proliferation, differentiation, migration, invasion and apoptosis, via post-transcriptionally regulating various target genes. A better understanding of the molecular mechanisms involved in miR-100-mediated tumor progression will provide an opportunity for exploring novel miR-100-based targeted therapies for human cancers. This review aims to summarize the recently published literature on the roles of miR-100 in regulating tumorigenesis, and explore its potential clinical applications for cancer diagnosis, prognosis and clinical treatment.

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“…miR-645 was upregulated in human adenocarcinoma of the gastric esophageal junction and inhibited apoptosis by targeting tumor suppressor IFIT2 (11). miR-100 promoted migration and invasion through mammalian target of rapamycin in esophageal squamous cell carcinoma (12). By contrast, miR-197 was downregulated in esophageal cancer with a poor prognosis, and may play a tumor-suppressor role (13).…”

Section: Introductionmentioning

confidence: 97%

MicroRNA-374a promotes esophageal cancer cell proliferation via Axin2 suppression

et al. 2015

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Abstract. is involved in the progress of various types of cancer, and may indicate a poor prognosis. However, its role in esophageal cancer remains to be determined. In the present study, the role of miR-374a in esophageal cancers and cancer cell growth was examined using miR-374a overexpression and underexpression models. The results showed that miR-374a was markedly increased in esophageal cancer cell lines and tumor samples from patients with esophageal cancer. In esophageal cancer Eca109 cells, the ectopic overexpression of miR-374a promoted cell growth. Additionally, cell growth was reduced by miR-374a inhibition. The mechanisms underlying the promotive role were examined and it was found that miR-374a significantly decreased the expression and transcription activity of axis inhibition protein 2 (Axin2). Axin2, a tumor suppressor, exhibited a marked inhibitory effect on Eca109 cell growth. The results identified a new role of miR-374a in esophageal cancer involving Axin2 suppression.

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MicroRNA-100 promotes migration and invasion through mammalian target of rapamycin in esophageal squamous cell carcinoma

Cited by 22 publications

References 39 publications

Stem Cell-Derived, microRNA-Carrying Extracellular Vesicles: A Novel Approach to Interfering with Mesangial Cell Collagen Production in a Hyperglycaemic Setting

Stem Cell-Derived, microRNA-Carrying Extracellular Vesicles: A Novel Approach to Interfering with Mesangial Cell Collagen Production in a Hyperglycaemic Setting

Multiple Roles of MicroRNA-100 in Human Cancer and its Therapeutic Potential

MicroRNA-374a promotes esophageal cancer cell proliferation via Axin2 suppression

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