An androgen-regulated miR-2909 modulates TGFβ signalling through AR/miR-2909 axis in prostate cancer

Ayub, Shiekh Gazalla; Kaul, Deepak; Ayub, Taha

doi:10.1016/j.gene.2017.07.037

Cited by 13 publications

(5 citation statements)

References 24 publications

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“…On the other hand, miR-2909 directly targets and reduces the expression of TGFBR2, which disables pSMAD2/3 activation, resulting in enhanced expressions of c-Myc and CCND1, reduced p21CIP, and escape of TGF-β suppressive effects on proliferation and viability. Furthermore, miR-2909 and androgen receptor are involved in a positive feedback regulation in which AR stimulates the expression of miR-2909 while miR-2909 enhances the expression of AR, providing further reinforcement of TGF-β signaling inhibition [321]. Strikingly, similar positive feedback was found between AR and miR-21, which targets and downregulates TGFBR2, preventing TGF-β antitumor activity [322].…”

Section: Prostate Cancermentioning

confidence: 96%

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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Section: Prostate Cancermentioning

confidence: 96%

TGF-β and microRNA Interplay in Genitourinary Cancers

Bogusławska¹,

Kryst

Poletajew

et al. 2019

Cells

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“…Another miRNA named miR-2909 promotes PCa by interacting with 3′-UTR of sequence of TGFRβR2 and resulting in its downregulation. Moreover, overexpression of miR-2909 also results in decreased expression of SMAD3, further verifying its role in tumor progression (Ayub et al, 2017). Recent advances in the field of phytochemistry have begun to scratch the surface of molecular oncology.…”

Section: Interplay Between Tgf-β Pathway and Mirnas In Pcamentioning

confidence: 80%

MicroRNAs and Natural Compounds Mediated Regulation of TGF Signaling in Prostate Cancer

et al. 2021

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Prostate cancer (PCa) is with rising incidence in male population globally. It is a complex anomaly orchestrated by a plethora of cellular processes. Transforming growth factor-beta (TGF-β) signaling is one of the key signaling pathways involved in the tumorigenesis of PCa. TGF-β signaling has a dual role in the PCa, making it difficult to find a suitable therapeutic option. MicroRNAs (miRNAs) mediated regulation of TGF-β signaling is responsible for the TGF-ß paradox. These are small molecules that modulate the expression of target genes and regulate cancer progression. Thus, miRNAs interaction with different signaling cascades is of great attention for devising new diagnostic and therapeutic options for PCa. Natural compounds have been extensively studied due to their high efficacy and low cytotoxicity. Here, we discuss the involvement of TGF-ß signaling in PCa with the interplay between miRNAs and TGF-β signaling and also review the role of natural compounds for the development of new therapeutics for PCa.

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“…Downregulation of TGF-β-R2 inhibits the expression of SMAD-dependent metastasis-promoting genes and invasion (54). High expression of TGF-β-R2 enhances PCa cell proliferation by promoting p-SMAD2/3/c-MYC signaling (60). TGF-β-R2 is associated with NF-κB and TGF-β signals to drive the progression, EMT and metastasis of castration-resistant PCa (61).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA SNHG16 functions as a tumor activator by sponging miR‑373‑3p to regulate the TGF‑β‑R2/SMAD pathway in prostate cancer

Weng

Liu

et al. 2021

Mol Med Rep

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Long non-coding RNAs (lncRNAs) are involved in the pathogenesis of prostate cancer (PCa) as competitive endogenous RNA. The present study aimed to investigate the molecular mech anisms of lncRNA small nucleolar RNA host gene 16 (SNHG16) in the proliferation and metastasis of PCa cells. Cancer tissues and adjacent normal tissues were collected from 80 patients with PCa who did not receive any treatment. Reverse transcription-quantitative PCR analysis was performed to detect the expression levels of SNHG16, hsa-microRNA (miRNA/miR)-373-3p and transforming growth factor-β receptor type 2 (TGF-β-R2), and Spearman's correlation coefficient analysis was performed to assess the correlations between these molecules. Furthermore, the effects of SNHG16 knockdown and overexpression on the biological functions of DU-145 PCa cells and TGF-β-R2/SMAD signaling were analyzed. The dual-luciferase reporter assay was performed to assess the associations between SNHG16 and miR-373-3p, and TGF-β-R2 and miR-373-3p, the effects of which were verified via rescue experiments. The results demonstrated that the expression levels of SNHG16 and TGF-β-R2 were significantly upregulated in PCa tissues, whereas miR-373-3p expression was significantly downregulated (P<0.001). In addition, negative correlations were observed between SNHG16 and miR-373-3p (rho, -0.631) and miR-373-3p and TGF-β-R2 (rho, -0.516). Overexpression of SNHG16 significantly promoted the proliferation, migration and invasion of PCa cells (P<0.05), and significantly increased the protein expression levels of TGF-β-R2, phosphorylated (p)-SMAD2, p-SMAD3, c-Myc and E2F4 (P<0.001). Notably, the results revealed that miR-373-3p is a target of SNHG16, and miR-373-3p knockdown rescued short hairpin (sh)-SNHG16-suppressed cellular functions by promoting TGF-β-R2/SMAD signaling. The results also revealed that miR-373-3p targets TGF-β-R2. Notably, transfection with miR-373-3p inhibitor rescued sh-TGF-β-R2-suppressed cell proliferation and migration. Taken together, the results of the present study suggest that SNHG16 promotes the proliferation and migration of PCa cells by targeting the miR-373-3p/TGF-β-R2/SMAD axis.

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An androgen-regulated miR-2909 modulates TGFβ signalling through AR/miR-2909 axis in prostate cancer

Cited by 13 publications

References 24 publications

TGF-β and microRNA Interplay in Genitourinary Cancers

TGF-β and microRNA Interplay in Genitourinary Cancers

MicroRNAs and Natural Compounds Mediated Regulation of TGF Signaling in Prostate Cancer

Long non‑coding RNA SNHG16 functions as a tumor activator by sponging miR‑373‑3p to regulate the TGF‑β‑R2/SMAD pathway in prostate cancer

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An androgen-regulated miR-2909 modulates TGFβ signalling through AR/miR-2909 axis in prostate cancer

Cited by 13 publications

References 24 publications

TGF-β and microRNA Interplay in Genitourinary Cancers

TGF-β and microRNA Interplay in Genitourinary Cancers

MicroRNAs and Natural Compounds Mediated Regulation of TGF Signaling in Prostate Cancer

Long non­‑coding RNA SNHG16 functions as a tumor activator by sponging miR‑373‑3p to regulate the TGF‑β‑R2/SMAD pathway in prostate cancer

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Long non‑coding RNA SNHG16 functions as a tumor activator by sponging miR‑373‑3p to regulate the TGF‑β‑R2/SMAD pathway in prostate cancer