miR-137 regulates epithelial-mesenchymal transition in gastrointestinal stromal tumor

Liu, Sheng; Cui, Juan; Liao, Guoqing; Zhang, Yi; Yao, Ke; Lu, Tailiang; Qi, Jing; Wan, Guohui

doi:10.1007/s13277-014-2177-5

Cited by 35 publications

(27 citation statements)

References 42 publications

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“…For example, Liu S etal . report that miR-137 regulates EMT and inhibits cell migration via down-regulation of Twist1 in gastrointestinal stromal tumor (52). Chen DL et al .…”

Section: Discussionmentioning

confidence: 99%

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

Zeng

Zhou

et al. 2016

Molecular Cancer Therapeutics

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Our recent studies found that isorhapontigenin (ISO) showed a significant inhibitory effect on human bladder cancer cell growth, accompanied with cell cycle G0/G1 arrest as well as down-regulation of Cyclin D1 expression at transcriptional level via inhibition of Sp1 transactivation in bladder cancer cells. In current studies, the potential ISO inhibition of bladder tumor formation has been explored in xenograft nude mouse model, and the molecular mechanisms underlying ISO inhibition of Sp1 expression and anti-cancer activities has been elucidated both in vitro and in vivo. Moreover, the studies demonstrated that ISO treatment induced the expression of miR-137, which in turn suppressed Sp1 protein translation by direct targeting Sp1 mRNA 3′UTR. Similar to ISO treatment, ectopic expression of miR-137 alone led to G0/G1 cell growth arrest and inhibition of anchorage-independent growth in human bladder cancer cells, which could be completely reversed by over-expression of GFP-Sp1. The inhibition of miR-137 expression attenuated ISO-induced the inhibition of Sp1/Cyclin D1 expression, and induction of G0/G1 cell growth arrest and suppression of cell anchorage-independent growth. Taken together, our studies have demonstrated that miR-137 induction by ISO targets Sp1 mRNA 3′UTR and inhibits Sp1 protein translation, which consequently results in reduction of Cyclin D1 expression, induction of G0/G1 growth arrest and inhibition of anchorage-independent growth in vitro and in vivo. Our results have provided novel insights into understanding the anti-cancer activity of ISO in the therapy of human bladder cancer.

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“…For example, Liu S etal . report that miR-137 regulates EMT and inhibits cell migration via down-regulation of Twist1 in gastrointestinal stromal tumor (52). Chen DL et al .…”

Section: Discussionmentioning

confidence: 99%

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

Zeng

Zhou

et al. 2016

Molecular Cancer Therapeutics

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“…Several miRNAs have been documented to directly inhibit TWIST1, including miR-1-1 [26], miR-33a [27, 28], miR-137 [29], miR-186 [30], miR-300 [31], miR-520d-5p [32], miR-539 [31], miR-543 [31], miR-675 [33], and miR-720 [34]. Most of these miRNAs repressed cancer cell EMT and metastasis in most examined cancer types, and some of them (miR-33a and miR-186) modulated cancer cell sensitivity to cisplatin by down-regulating TWIST1 [27, 30].…”

Section: Discussionmentioning

confidence: 99%

miR-151-3p Targets TWIST1 to Repress Migration of Human Breast Cancer Cells

Yeh¹,

Huang²,

Yeh³

et al. 2016

PLoS ONE

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TWIST1 is a highly conserved basic helix-loop-helix transcription factor that contributes to cancer metastasis by promoting an epithelial-mesenchymal transition and repressing E-cadherin gene expression in breast cancer. In this study, we explored the potential role of miR-151 in TWIST1 expression and cancer properties in human breast cancer cells. We found that the human TWIST1 3’UTR contains a potential binging site for miR-151-3p at the putative target sequence 5’-CAGUCUAG-3’. Using a TWIST1-3’UTR luciferase reporter assay, we demonstrated that the target sequence within the TWIST1 3’UTR is required for miR-151-3p regulation of TWIST1 expression. Moreover, we found that ectopic expression of miR-151-3p by infection with adenoviruses expressing miR-151 significantly decreased TWIST1 expression, migration and invasion, but did not affect cell growth and tumorsphere formation of human breast cancer cells. In addition, overexpression of the protein coding region without the 3’UTR of TWIST1 reversed the repression of cell migration by miR-151-3p. Furthermore, knockdown of miR-151-3p increased TWIST1 expression, reduced E-cadherin expression, and enhanced cell migration. In conclusion, these results suggest that miR-151-3p directly regulates TWIST1 expression by targeting the TWIST1 3’UTR and thus repressing the migration and invasion of human breast cancer cells by enhancing E-cadherin expression. Our findings add to accumulating evidence that microRNAs are involved in breast cancer progression by modulating TWIST1 expression.

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“…The expression of FGF2, a ligand of FGFR3, is increased in imatinib‐resistant GIST. In adition, the proliferation and metastatic activity are in part regulated by miRNAs, such as miR‐34a , miR‐335 and miR‐137 . The expression of immune‐related molecules such as T cell activation antigen (CD26) and programmed cell death ligand 1 (PDL1) are predictable for the prognosis .…”

Section: Clinical Practice For Wild Type Gistmentioning

confidence: 99%

“…In adition, the proliferation and metastatic activity are in part regulated by miRNAs, such as miR-34a, miR-335 and miR-137. 33,34 The expression of immunerelated molecules such as T cell activation antigen (CD26) and programmed cell death ligand 1 (PDL1) are predictable for the prognosis. 35,36 The enhanced expression of CD26 and the reduced expression of PDL1 are associated with higher risk of metastasis.…”

Section: New Strategies Of Targeting Therapymentioning

confidence: 99%

“Wild type” GIST: Clinicopathological features and clinical practice

Wada

Arai

Kure

et al. 2016

Pathology International

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Gastrointestinal stromal tumor (GIST) is a mesenchymal tumor of the gastrointestinal tract. Mutation of KIT and PDGFRA genes is implicated in the tumorigenesis. Approximately 10% of GISTs do not harbor mutation of these genes, and they are designated as "wild type" GIST. They are classified into succinate dehydrogenase (SDH)-deficient and non-SDH-deficient groups. SDH-deficient group includes Carney triad and Carney Stratakis syndrome. The patients are young women. Tumors occur in the antrum of the stomach, and tumor cells are epithelioid. Lymph node metastasis is frequent. The non-SDH-deficient group includes neurofibromatosis (NF) type 1 and GISTs with mutations of BRAF, KRAS, and PIK3CA and with the ETV6-NTRK3 fusion gene. GIST in NF occurs in the small intestine, and tumor cells are spindle shaped. GIST with BRAF mutation arises in the small intestine. Attention to the age, gender, family history and other neoplasms may raise the prediction of syndromic disease. Location of the tumor, morphology, and pleomorphism of the tumor cells are further informative. Lymphovascular invasion should be carefully evaluated. The determination of KIT expression is essential for the diagnosis. When wild type GIST is suspected, intensive genetic analysis is required. Further, a careful and long-time observation is recommended.

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miR-137 regulates epithelial-mesenchymal transition in gastrointestinal stromal tumor

Cited by 35 publications

References 42 publications

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

miR-151-3p Targets TWIST1 to Repress Migration of Human Breast Cancer Cells

“Wild type” GIST: Clinicopathological features and clinical practice

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