TGF-beta induced RBL2 expression in renal cancer cells by down-regulating miR-93

Shi, Jing; Zhuang, Yong; Liu, X. K.; Zhang, Y. X.; Zhang, Y.

doi:10.1007/s12094-014-1185-7

Cited by 14 publications

(8 citation statements)

References 23 publications

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“…miR-93, a microRNA frequently associated with TGF-β signaling in controlling cell cycle arrest [ 26 ], cell proliferation, and differentiation [ 27 ], was also down-regulated in both Groups A and B. Moreover, we discovered that miR-1224 and miR-125a-3p, which were initially up-regulated in Group A, became down-regulated at day 3 and 5 in Group B post-induced with IGF-1.…”

Section: Discussionmentioning

confidence: 92%

MicroRNA Expression Profile of Neural Progenitor-Like Cells Derived from Rat Bone Marrow Mesenchymal Stem Cells under the Influence of IGF-1, bFGF and EGF

Huat

Khan

Abdullah

et al. 2015

IJMS

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Insulin-like growth factor 1 (IGF-1) enhances cellular proliferation and reduces apoptosis during the early differentiation of bone marrow derived mesenchymal stem cells (BMSCs) into neural progenitor-like cells (NPCs) in the presence of epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF). BMSCs were differentiated in three groups of growth factors: (A) EGF + bFGF, (B) EGF + bFGF + IGF-1, and (C) without growth factor. To unravel the molecular mechanisms of the NPCs derivation, microarray analysis using GeneChip® miRNA arrays was performed. The profiles were compared among the groups. Annotated microRNA fingerprints (GSE60060) delineated 46 microRNAs temporally up-regulated or down-regulated compared to group C. The expressions of selected microRNAs were validated by real-time PCR. Among the 46 microRNAs, 30 were consistently expressed for minimum of two consecutive time intervals. In Group B, only miR-496 was up-regulated and 12 microRNAs, including the let-7 family, miR-1224, miR-125a-3p, miR-214, miR-22, miR-320, miR-708, and miR-93, were down-regulated. Bioinformatics analysis reveals that some of these microRNAs (miR-22, miR-214, miR-125a-3p, miR-320 and let-7 family) are associated with reduction of apoptosis. Here, we summarize the roles of key microRNAs associated with IGF-1 in the differentiation of BMSCs into NPCs. These findings may provide clues to further our understanding of the mechanisms and roles of microRNAs as key regulators of BMSC-derived NPC maintenance.

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Section: Discussionmentioning

confidence: 92%

MicroRNA Expression Profile of Neural Progenitor-Like Cells Derived from Rat Bone Marrow Mesenchymal Stem Cells under the Influence of IGF-1, bFGF and EGF

Huat

Khan

Abdullah

et al. 2015

IJMS

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“…Shi, et al found that TGF-β induces RBL2 expression and arrests renal cancer cell growth by downregulating miR-93-5p, and indirectly showed that miR-93-5p suppression induces G1 phase arrest. Wulfken, et al demonstrated that miR-93-5p is upregulated in renal cancer patient serum and tissues, but the miR-93-5p function was not well understood [ 15 , 16 ].…”

Section: Discussionmentioning

confidence: 99%

miR-93-3p inhibition suppresses clear cell renal cell carcinoma proliferation, metastasis and invasion

et al. 2017

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miRNA dysregulation is associated with many human diseases, including cancer. This study explored the effects of miR-93-3p on clear cell renal cell carcinoma (ccRCC). We found that miR-93-3p is upregulated an average of 38-fold in 138 ccRCC specimens compared to matched normal kidney tissues, which correlated with poor patient outcome. miR-93-3p inhibition reduced ccRCC cell growth, invasion, and migration in vitro and in a mouse xenograft model. A search of the TargetScan, miRanda, and PicTar databases revealed that miR-93-3p is predicted to regulate pigment epithelium-derived factor (PEDF). A direct PEDF-miR-93-3p interaction was confirmed via dual-luciferase reporter assays. Like miR-93-3p inhibition, PEDF overexpression induced cell apoptosis and inhibited migration and invasion. Additionally, co-transfection with PEDF siRNA reversed the effects of miR-93-3p inhibition in ccRCC cells. Thus, miR-93-3p is a likely ccRCC oncogene that acts by regulating PEDF. These results suggest that miR-93-3p may predict ccRCC patient clinical outcome and serve as a novel anti-ccRCC therapeutic target.

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“…Consequently, miR-93 abolishes tumor-suppressive TGF-β1 effects, providing an explanation for TGF-β1 resistance in RCC. Intriguingly, TGF-β1 reduces miR-93 expression, which leads to increased RBL2 expression, indicating reciprocal feedback regulation in the TGF-β1-RBL2-miR-93 axis [287]. Furthermore, miR-429 disrupts TGF-β-dependent inhibition of E-cadherin expression, suggestive of an attenuation of TGF-β-induced EMT.…”

Section: Renal Cancermentioning

confidence: 97%

TGF-β and microRNA Interplay in Genitourinary Cancers

Bogusławska¹,

Kryst

Poletajew

et al. 2019

Cells

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Genitourinary cancers (GCs) include a large group of different types of tumors localizing to the kidney, bladder, prostate, testis, and penis. Despite highly divergent molecular patterns, most GCs share commonly disturbed signaling pathways that involve the activity of TGF-β (transforming growth factor beta). TGF-β is a pleiotropic cytokine that regulates key cancer-related molecular and cellular processes, including proliferation, migration, invasion, apoptosis, and chemoresistance. The understanding of the mechanisms of TGF-β actions in cancer is hindered by the “TGF-β paradox” in which early stages of cancerogenic process are suppressed by TGF-β while advanced stages are stimulated by its activity. A growing body of evidence suggests that these paradoxical TGF-β actions could result from the interplay with microRNAs: Short, non-coding RNAs that regulate gene expression by binding to target transcripts and inducing mRNA degradation or inhibition of translation. Here, we discuss the current knowledge of TGF-β signaling in GCs. Importantly, TGF-β signaling and microRNA-mediated regulation of gene expression often act in complicated feedback circuits that involve other crucial regulators of cancer progression (e.g., androgen receptor). Furthermore, recently published in vitro and in vivo studies clearly indicate that the interplay between microRNAs and the TGF-β signaling pathway offers new potential treatment options for GC patients.

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TGF-beta induced RBL2 expression in renal cancer cells by down-regulating miR-93

Abstract: TGF-beta induced RBL2 expression through down-regulating miR-93 in renal cancer cells. The newly identified TGF-beta/miR-93/RBL2 signal pathway reveals a new mechanism of TGF-beta induced growth arrest in renal cancer.

Cited by 14 publications

References 23 publications

MicroRNA Expression Profile of Neural Progenitor-Like Cells Derived from Rat Bone Marrow Mesenchymal Stem Cells under the Influence of IGF-1, bFGF and EGF

MicroRNA Expression Profile of Neural Progenitor-Like Cells Derived from Rat Bone Marrow Mesenchymal Stem Cells under the Influence of IGF-1, bFGF and EGF

miR-93-3p inhibition suppresses clear cell renal cell carcinoma proliferation, metastasis and invasion

TGF-β and microRNA Interplay in Genitourinary Cancers

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