Androgen-regulated miR-32 targets BTG2 and is overexpressed in castration-resistant prostate cancer

Jalava, Sanni E.; Urbanucci, Alfonso; Latonen, Leena; Waltering, Kati K.; Sahu, Biswajyoti; Jänne, Olli A.; Seppälä, Janne; Lähdesmäki, Harri; Tammela, Teuvo L.J.; Visakorpi, Tapio

doi:10.1038/onc.2011.624

Cited by 202 publications

(186 citation statements)

References 46 publications

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“…Previous research reported that miR-590-5p, another arm of hsa-miR-590, 20 was significantly overexpressed in CRPC. 21 Further studies indicated that ectopic expression of miR-590-3p dramatically promoted, whereas suppression of endogenous miR-590-3p attenuated the proliferation and invasion of LNCaP and C4-2 cells. Moreover, miR-590-3p mimics accelerated the growth of xenografted tumors.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-590-3p promotes cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells

Chen

Luo

2017

Tumour Biol.

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Inositol polyphosphate 4-phosphatase type II emerges as a tumor suppressor in prostate cancer, and its loss of expression is associated with poor prognosis for prostate cancer. However, the mechanism of downregulation of inositol polyphosphate 4-phosphatase type II in prostate cancer development has not yet been fully clarified. In this study, microRNA-590-3p was found to be upregulated in both prostate cancer tissues and cell lines. Overexpression of microRNA-590-3p by microRNA-590-3p mimics promoted prostate cancer cell proliferation and invasion and accelerated the growth of xenografted tumors, while microRNA-590-3p inhibitors contributed to inhibition of cellular proliferation and invasion as well as tumor growth. A dual-luciferase reporter assay and expression analysis further confirmed that inositol polyphosphate 4-phosphatase type II was a direct target of microRNA-590-3p. Enforced expression of microRNA-590-3p led to repression of inositol polyphosphate 4-phosphatase type II messenger RNA and protein expression, as well as upregulation of p-Akt, p-FoxO3a, and cyclin D1 and downregulation of p21 expression in prostate cancer cell lines. Overexpression of inositol polyphosphate 4-phosphatase type II could reduce microRNA-590-3p-induced cell proliferation and invasion as well as tumor growth, and decrease microRNA-590-3p-mediated upregulation of cyclin D1 and downregulation of p21 expression in prostate cancer cells. Taken together, our findings reveal that microRNA-590-3p is a potential onco-microRNA that participates in carcinogenesis of human prostate cancer by suppressing inositol polyphosphate 4-phosphatase type II expression and involving the Akt/FoxO3a pathway. MicroRNA-590-3p may represent a potential therapeutic target for prostate cancer patients.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-590-3p promotes cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells

Chen

Luo

2017

Tumour Biol.

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“…Additionally, it has been reported that miR-32 was significantly down-regulated in osteosarcoma tissues, compared with the adjacent normal tissues, and it could inhibit osteosarcoma cell proliferation and invasion by targeting Sox9 [15]. However, Jalava et al found that miR-32 was overexpressed in castration-resistant prostate cancer and targeted BTG2 [16]. Wu and colleagues reported that miR-32 overexpression was correlated with specific colorectal cancer clinicopathological features and may be a marker of poor prognosis in colorectal cancer patients, miR-32 and phosphatase and tensin homolog (PTEN) expression were inversely correlated, and further identified PTEN as the functional downstream target of miR-32 by directly targeting the 3′-UTR of PTEN [17,18].…”

Section: Introductionmentioning

confidence: 93%

MiR-32 induces cell proliferation, migration, and invasion in hepatocellular carcinoma by targeting PTEN

Yan

Chen

et al. 2015

Tumor Biol.

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MicroRNAs (miRNAs) regulate gene expression by inhibiting translation of target messenger RNAs (mRNAs) through pairing with miRNA recognition elements (MREs), usually in 3'-UTRs. miRNAs are involved in the pathogenesis of several types of cancers. Specifically, microRNA-32 (miR-32) is overexpressed in colorectal carcinoma, wherein accumulating evidence indicates that it functions as an oncogene. However, the function of miR-32 in hepatocellular carcinoma (HCC) has not been totally elucidated. In the present study, we found the expression of miR-32 was up-regulated in HCC tissue and cell lines, inversely the expression of phosphatase and tensin homolog (PTEN) decreased. Besides, miRNA-32 down-regulates PTEN through binding to 3'-UTR of PTEN mRNA from luciferase reporter assay, and the expression level of miR-32 could affect the proliferation, migration, and invasion of liver cancer cell lines via PTEN/Akt signaling pathway. Down-expression of PTEN could significantly attenuate the inhibitory effects of knockdown miR-32 on the proliferation, migration, and invasion of liver cancer cells, suggesting that miR-32 could be a potential target for HCC treatment.

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“…Another family member, miR-32, induced by androgen, is overexpressed in castration-resistant prostate cancer, thus leading to reduced expression of BTG2, which is associated with a short progression-free time in patients who underwent prostatectomy (42). miR-32 can also regulate the lipid metabolism of oligodendrocytes and myelin by targeting SLC45A3 (61).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-92a Negatively Regulates Toll-like Receptor (TLR)-triggered Inflammatory Response in Macrophages by Targeting MKK4 Kinase

Lai

Song

Liu

et al. 2013

Journal of Biological Chemistry

117

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Background: microRNAs (miRNAs) participate in innate immune responses. Results: miR-92a decreases rapidly in macrophages once stimulated with TLR ligands, and miR-92a controls inflammatory response by targeting MKK4/JNK/c-Jun pathway. Conclusion: TLR-mediated miR-92a reduction feedback enhances TLR-triggered inflammatory response. Significance: Our findings reveal a novel positive feedback loop in which TLR-reduced miR-92a expression functions to regulate the innate inflammatory responses.

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Androgen-regulated miR-32 targets BTG2 and is overexpressed in castration-resistant prostate cancer

Cited by 202 publications

References 46 publications

MicroRNA-590-3p promotes cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells

MicroRNA-590-3p promotes cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells

MiR-32 induces cell proliferation, migration, and invasion in hepatocellular carcinoma by targeting PTEN

MicroRNA-92a Negatively Regulates Toll-like Receptor (TLR)-triggered Inflammatory Response in Macrophages by Targeting MKK4 Kinase

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