Transforming growth factor-β promotes prostate bone metastasis through induction of microRNA-96 and activation of the mTOR pathway

Mk, Siu; Tsai, Yu-Chen; Chang, Yung-Fu; Jj, Yin; Suau, Florent; Wy, Chen; Yn, Liu

doi:10.1038/onc.2014.414

Cited by 76 publications

(59 citation statements)

References 38 publications

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“…miR-183 promotes tumor invasion and metastasis by targeting PDCD4, protein phosphatase 2A (PP2A), EGR1 and PTEN [76, 78, 104, 105]. In addition, TGF-β and Smad can also promote prostate cancer bone metastasis by induction of miR-96 and activation of the mTOR pathway [106]. Moreover, the inhibitory effect on metastasis in hepatoma carcinoma cells, induced by the suppression of miR-96 [107], was reported as being associated with the inhibition of EFNA5 expression by miR-96-targeting [85].…”

Section: Resultsmentioning

confidence: 99%

Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Liang

Fan

et al. 2016

Oncotarget

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Previous studies have reported aberrant expression of the miR-183-96-182 cluster in a variety of tumors, which indicates its' diagnostic or prognostic value. However, a key characteristic of the miR-183-96-182 cluster is its varied expression levels, and pleomorphic functional roles in different tumors or under different conditions. In most tumor types, the cluster is highly expressed and promotes tumorigenesis, cancer progression and metastasis; yet tumor suppressive effects have also been reported in some tumors. In the present study, we discuss the upstream regulators and the downstream target genes of miR-183-96-182 cluster, and highlight the dysregulation and functional roles of this cluster in various tumor cells. Newer insights summarized in this review will help readers understand the different facets of the miR-183-96-182 cluster in cancer development and progression.

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Section: Resultsmentioning

confidence: 99%

Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Liang

Fan

et al. 2016

Oncotarget

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“…miR-96 directly targets AKT1S1 that encodes for PRAS40, a negative regulator of mTOR kinase, which prevents the binding of mTOR to its substrates [107] . miR-96 upregulation in prostate cancer cells has also been shown to lead to the downregulation of the AKT1S1, thereby unleashing mTOR signaling to promote prostate bone metastasis [108] .…”

Section: Mirnas That Activate Mtor Pathwaymentioning

confidence: 99%

Emerging Role of MicroRNAs in mTOR Signaling

Zhang

Huang

Wang³

et al. 2017

Cell. Mol. Life Sci.

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Mechanistic target of rapamycin (mTOR) is a conserved serine/threonine kinase that plays a critical role in the control of cellular growth and metabolism. Hyperactivation of mTOR pathway is common in human cancers, driving uncontrolled proliferation. MicroRNA (miRNA) is a class of short noncoding RNAs that regulate the expression of a wide variety of genes. Deregulation of miRNAs is a hallmark of cancer. Recent studies have revealed interplays between miRNAs and the mTOR pathway during cancer development. Such interactions appear to provide a fine-tuning of various cellular functions and contribute qualitatively to the behavior of cancer. Here we provide an overview of current knowledge regarding the reciprocal relationship between miRNAs and mTOR pathway: regulation of mTOR signaling by miRNAs and control of miRNA biogenesis by mTOR. Further research in this area may prove important for the diagnosis and therapy of human cancer.

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“…We cannot rule out the possibility that the WNT pathway may also contribute to miR-182 cluster expression in melanomas with different genetic background or molecular contexts. Another set of reports propose that the growth factor TGF-β regulates the expression of the miR-182 cluster in glioma [26], gallbladder cancer metastasis [27], prostate cancer bone metastasis [28] and breast cancer [29] but the specific mediators of TGFβ effects were not identified. In melanoma, TGF-β has also been shown to exert tumor promoting functions boosting cell motility and invasiveness [30].…”

Section: Discussionmentioning

confidence: 99%

Krüppel-like factor 4 (KLF4) regulates the miR-183~96~182 cluster under physiologic and pathologic conditions

Segura

Jubierre

et al. 2017

Oncotarget

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MicroRNAs (miRNAs) are a class of endogenous non-coding small RNAs that post-transcriptionally control the translation and stability of target mRNAs in a sequence-dependent manner. MiRNAs are essential for key cellular processes including proliferation, differentiation, cell death and metabolism, among others. Consequently, alterations of miRNA expression contribute to developmental defects and a myriad of diseases.The expression of miRNAs can be altered by several mechanisms including gene copy number alterations, aberrant DNA methylation, defects of the miRNA processing machinery or unscheduled expression of transcription factors. In this work, we sought to analyze the regulation of the miR-182 cluster, located at the 7q32 locus, which encodes three different miRNAs that are abundantly expressed in human embryonic stem cells and de-regulated in cancer. We have found that the Krüppel-like factor 4 (KLF4) directly regulates miR-182 cluster expression in human embryonic stem cells (hESCs) and in melanoma tumors, in which the miR-182 cluster is highly expressed and has a pro-metastatic role. Furthermore, higher KLF4 expression was found to be associated with metastatic progression and poor patient outcome. Loss of function experiments revealed that KLF4 is required for melanoma cell maintenance. These findings provide new insights into the regulation of the miR-182 cluster expression and new opportunities for therapeutic intervention in tumors in which the KLF4-miR-182 cluster axis is deregulated.

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Transforming growth factor-β promotes prostate bone metastasis through induction of microRNA-96 and activation of the mTOR pathway

Cited by 76 publications

References 38 publications

Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Dysregulation and functional roles of miR-183-96-182 cluster in cancer cell proliferation, invasion and metastasis

Emerging Role of MicroRNAs in mTOR Signaling

Krüppel-like factor 4 (KLF4) regulates the miR-183~96~182 cluster under physiologic and pathologic conditions

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