Structure and function of FUS gene in prostate cancer

Ghanbarpanah, E; Kohanpour, M A; Hosseini-Beheshti, F; Yari, L; Keshvari, Mahrokh

doi:10.4149/bll_2018_118

Cited by 10 publications

(11 citation statements)

References 21 publications

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“…FUS was a multifunctional protein and participated in many RNA metabolism pathways, and mutant FUS suppressed protein biosynthesis and disrupted NMD regulation (Kamelgarn et al, 2018). FUS expression was also inversely correlated with Gleason grade of prostate cancer (Ghanbarpanah et al, 2018). We demonstrated that deregulation of FUS and UPF1 was in both PC3 and DU145 cells following knockdown of RP11-423H2.3 or LAMTOR5-AS1 ( Figure S4).…”

Section: Discussionmentioning

confidence: 81%

“…As FUS is a member of the TET protein family, this protein was found to be inversely regulated by miR-141 in human neuroblastoma (Wang et al, 2016) and can be activated by lncRNA XIST, which also served as a ceRNA in cervical cancer progression while competitively binding with miR-200a (Zhu et al, 2018). FUS promoted conditions that favored cell-cycle arrest by reducing proliferator factors and was a key link between androgen receptor signaling and the progression of the cell cycle in prostate cancer (Brooke et al, 2011;Ghanbarpanah et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

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Identification of Specific Long Non-Coding Ribonucleic Acid Signatures and Regulatory Networks in Prostate Cancer in Fine-Needle Aspiration Biopsies

Zheng

Xia

et al. 2020

Front. Genet.

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Prostate cancer (PCa) is one of the most common tumors in men and can be lethal, especially if left untreated. A substantial majority of PCa patients not only are diagnosed based on fine needle aspiration (FNA) biopsies, but their treatment choices are also largely driven by the pathological findings obtained with these FNA specimens. It is widely believed that lncRNAs have strong biological significance, but their specific functions and regulatory networks have not been elucidated. LncRNAs may serve as key players and regulators of PCa carcinogenesis and could be novel biomarkers of this cancer. To identify potential markers for early detection of PCa, in this study, we employed a competing endogenous RNA (ceRNA) microarray to identify differentially expressed lncRNAs (DelncRNAs) in PCa tissue and quantitative real-time PCR (qRT-PCR) analysis to validate these DelncRNAs in FNA biopsies. We demonstrated that a total of 451 lncRNAs were differentially expressed in four pairs of PCa/adjacent tissues, and upregulation of the lncRNAs RP11-33A14.1, RP11-423H2.3, and LAMTOR5-AS1 was confirmed in FNA biopsies of PCa by qRT-PCR and was consistent with the ceRNA array data. The association between the expression of the lncRNA LAMTOR5-AS1 and aggressive cancer was also investigated. Regulatory network analysis of DelncRNAs showed that the lncRNAs RP11-33A14.1 and RP11-423H2.3 targeted miR-7, miR-24-3p, and miR-30 and interacted with the RNA binding protein FUS. Knockdown of these DelncRNAs in PCa cells also demonstrated the effects of RP11-423H2.3 on miR-7/miR-24/miR-30 or LAMTOR5-AS1 on miR-942-5p/miR-542-3p via direct interaction. The results of these studies indicate that these three specific lncRNA signatures and regulatory

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Identification of Specific Long Non-Coding Ribonucleic Acid Signatures and Regulatory Networks in Prostate Cancer in Fine-Needle Aspiration Biopsies

Zheng

Xia

et al. 2020

Front. Genet.

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“…Researches displayed that PCa patients with higher FUS levels have the chance of more survival. 23 Furthermore, increased expression of FUS reduces tumor growth and prevents the G1 stage and increases apoptosis in PCa cells. 23 In this study, we found that EMX2OS directly bound with FUS protein, and played synergy effect with FUS protein: the cell proliferation, migration, invasion and tumor growth were decreased, and PKG1 and PKG2 expression and cGMP concentration were increased after the co-transfection of EMX2OS and FUS, compared with the FUS transfection group.…”

Section: Discussionmentioning

confidence: 99%

“…23 Furthermore, increased expression of FUS reduces tumor growth and prevents the G1 stage and increases apoptosis in PCa cells. 23 In this study, we found that EMX2OS directly bound with FUS protein, and played synergy effect with FUS protein: the cell proliferation, migration, invasion and tumor growth were decreased, and PKG1 and PKG2 expression and cGMP concentration were increased after the co-transfection of EMX2OS and FUS, compared with the FUS transfection group. The effect of EMX2OS siRNA and FUS siRNA co-treatment on cell proliferation, migration, invasion, cGMP-PKG pathway and tumor growth was stronger than the effect of FUS siRNA transfection.…”

Section: Discussionmentioning

confidence: 99%

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<p>LncRNA EMX2OS, Regulated by TCF12, Interacts with FUS to Regulate the Proliferation, Migration and Invasion of Prostate Cancer Cells Through the cGMP-PKG Signaling Pathway</p>

Wang¹,

Zhang²,

Chang³

et al. 2020

OTT

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Background LncRNA EMX2OS (EMX2 opposite strand/antisense RNA) is notably downregulated in prostate cancer (PCa) tissues and may be regarded as a potential molecular biomarker for diagnosis and prognosis. However, its exact role in regulating the development of PCa is obscure. Methods The EMX2OS expression was assessed in PCa tissues, paracancer tissues, PCa cells and normal prostate epithelial cells by qPCR. Gain- and loss-of-function experiments were performed to investigate the role of EMX2OS and FUS in cGMP-PKG (cyclic guanosine monophosphate-dependent protein kinase)-mediated proliferation, invasion, and migration in human PCa cell lines DU145 and PC3. Then, the interaction of transcription factor 12 (TCF12) with EMX2OS promoter was confirmed by using the dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. RNA binding protein immunoprecipitation and RNA pull-down assays were used to verify the interaction between EMX2OS and FUS protein. Finally, the role of EMX2OS and FUS in tumor growth in vivo was validated in a xenograft nude mouse model. Results TCF12 and EMX2OS were both downregulated in PCa tissues and cells, and they negatively regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. TCF12 was a transcription factor of EMX2OS. TCF12 and EMX2OS overexpression both down-regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. Furthermore, EMX2OS directly bound with FUS protein and had a synergy effect with FUS protein on cGMP-PKG-mediated cell functions, which could be suppressed by (D)-DT-2 (a cGMP-PKG inhibitor). In addition, the overexpression of FUS or EMX2OS individually markedly decreased the volume and weight of tumors in vivo, and co-overexpression of them further inhibited tumor growth. Conclusion EMX2OS, transcriptionally regulated by TCF12, played a synergy role with FUS protein in regulating the proliferation, migration and invasion of PCa cells by activating the cGMP-PKG pathway.

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The lncRNA HOTAIR attenuates pyroptosis of diabetic cardiomyocytes by recruiting FUS to regulate SIRT3 expression

Xiong

Zhou

2023

The Kaohsiung J of Med Scie

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Diabetic cardiomyopathy (DCM) is a serious cardiovascular complication of diabetes that severely affects the quality of life of diabetic patients. Long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of DCM. However, the role of the lncRNA homeobox transcript antisense RNA (HOTAIR) in the progression of DCM remains unclear. The present study aimed to investigate the role of HOTAIR in high glucose (HG)-induced pyroptosis in cardiomyocytes. The expression of the lncRNA HOTAIR, FUS, and SIRT3 in H9C2 cardiomyocytes was detected by RT-qPCR. Western blotting was used to evaluate the expression of FUS and SIRT3 as well as that of pyroptosis-and inflammation-related proteins. RT-qPCR and ELISA were used to determine the expression and secretion of IL-1β and IL-18. RNA pulldown and RIP experiments were used to validate the binding relationship among HOTAIR, FUS, and SIRT3. Flow cytometry was performed to detect pyroptosis. HG induced pyroptosis and elevated the expression of proteins associated with pyroptosis and inflammation (NLRP3, GSDMD-N, cleaved caspase-1, IL-1β, and IL-18) in cardiomyocytes. HOTAIR and SIRT3 levels were decreased in HG-exposed H9C2 cells. Additionally, overexpression of HOTAIR inhibited the HG-induced pyroptosis and inflammatory response in cardiomyocytes. HOTAIR upregulated SIRT3 expression in H9C2 cells by targeting FUS. Moreover, SIRT3 upregulation suppressed HG-mediated pyroptosis of cardiomyocytes. Notably, SIRT3 depletion reversed the inhibitory effect of HOTAIR on HGtriggered pyroptosis in cardiomyocytes. Our research indicates that HOTAIR alleviates pyroptosis in diabetic cardiomyocytes through the FUS/SIRT3 axis, providing a potential marker for the diagnosis and treatment of DCM.

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Structure and function of FUS gene in prostate cancer

Cited by 10 publications

References 21 publications

Identification of Specific Long Non-Coding Ribonucleic Acid Signatures and Regulatory Networks in Prostate Cancer in Fine-Needle Aspiration Biopsies

Identification of Specific Long Non-Coding Ribonucleic Acid Signatures and Regulatory Networks in Prostate Cancer in Fine-Needle Aspiration Biopsies

<p>LncRNA EMX2OS, Regulated by TCF12, Interacts with FUS to Regulate the Proliferation, Migration and Invasion of Prostate Cancer Cells Through the cGMP-PKG Signaling Pathway</p>

The lncRNA HOTAIR attenuates pyroptosis of diabetic cardiomyocytes by recruiting FUS to regulate SIRT3 expression

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