Crosstalk between the lnc<scp>RNA UCA</scp>1 and micro<scp>RNA</scp>s in cancer

Xuan, Wei; Yu, Hongyu; Zhang, Xiaoling; Song, Dandan

doi:10.1002/1873-3468.13470

Cited by 37 publications

(23 citation statements)

References 141 publications

(210 reference statements)

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“…The Long non-coding RNA UCA1 was located in chromosome 9p13.12, and has been found to be overexpressed in tumor tissues, such as esophageal squamous cell carcinoma,colorectal cancer, ovarian cancer, bile duct carcinoma and melanoma etc. [16][17][18][19][20][21][22][23].UCA1 are participated in the tumorigenesis and progression, functioning as an oncogene [24][25][26][27][28][29][30]. However, the relation between UCA1 and renal cancer is still unknown and mysterious particularly.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidences suggested that long non-coding RNAs (lncRNAs) perform important or vital functions in the malignant tumors [9][10][11][12][13][14][15]. LncRNA urothelial cancer associated 1 (UCA1) is abnormally expressed in esophageal squamous cell carcinoma, colorectal cancer, gastric cancer melanoma cells, pancreatic cancer, thyroid cancer, lung cancer and so on [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]. In vitro and in vivo assays were conducted to further explore its underlying roles in tumor progression.…”

Section: Introductionmentioning

confidence: 99%

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Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Wang

et al. 2020

Mol Cancer

102

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Background: Accumulating literatures have indicated that long non-coding RNAs (lncRNAs) are potential biomarkers that play key roles in tumor development and progression. Urothelial cancer associated 1 (UCA1) is a novel lncRNA that acts as a potential biomarker and is involved in the development of cancers. However, the molecular mechanism of UCA1 in renal cancer is still needed to further explore. Methods: The relative expression level of UCA1 was determined by Real-Time qPCR in a total of 88 patients with urothelial renal cancer and in different renal cancer cell lines. Loss-of-function experiments were performed to investigate the biological roles of UCA1 and miR-182-5p on renal cancer cell proliferation, migration, apoptosis and tumorigenicity. Comprehensive transcriptional analysis, dual-luciferase reporter assay and western blot etc. were performed to explore the molecular mechanisms underlying the functions of UCA1. Results: In this study, we found that UCA1 was significantly up-regulated in renal cancer. Moreover, increased UCA1 expression was positively correlated with differentiation and advanced TNM stage. Further experiments demonstrated that knockdown of UCA1 inhibited malignant phenotypes and Notch signal path of renal cancer cells, and miR-182-5p was reverse function as UCA1. UCA1 functioned as a miRNA sponge to positively regulate the expression of Delta-like ligand 4(DLL4) through sponging miR-182-5p and subsequently promoted malignant phenotypes of renal cancer cells, thus UCA1 playing an oncogenic role and miR-182-5p as an antioncogenic one in renal cancer pathogenesis. Conclusion: UCA1-miR-182-5p-DLL4 axis is involved in proliferation and progression of renal cancer. Thus, this study demonstrated that UCA1 plays a critical regulatory role in renal cancer cell and UCA1 may serve as a potential diagnostic biomarker and therapeutic target of renal cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Wang

et al. 2020

Mol Cancer

102

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“…The prediction is consistent with the associations of UCA1 with reductions in the 5-year disease-free survival in PC (n=130; HR, 2.88; 95% CI, 1.36-6.21; P= 0.007) (200) and in overall survival (n=40, P<0.001) (201). Additionally, the upregulation of UCA1 has also been shown to be a risk factor for the progression of ovarian cancer (202), gastric cancer (203), melanoma (204), pancreatic cancer (205), glioma (206) and others (207). Mechanistically, UCA1 facilitates PC at least in part through upregulations of ATF2 and CXCR4 by sponging miR-204 (208,209).…”

Section: Gene Expression-based Biomarkersmentioning

confidence: 99%

“…Mechanistically, UCA1 facilitates PC at least in part through upregulations of ATF2 and CXCR4 by sponging miR-204 (208,209). Intriguingly, UCA1 sequesters miR-204, leading to EMT in glioma, TGF-β signaling in oral cancer and Sox4 actions in esophageal cancer (207); UCA1 also sponges other miRNAs in promoting tumorigenesis in other cancer types (207). In this regard, the association of UCA1 with BCR could be strengthened by consideration of UCA1-regulated oncogenic factors.…”

Section: Gene Expression-based Biomarkersmentioning

confidence: 99%

Assessment of biochemical recurrence of prostate cancer (Review)

Lin

Kapoor

et al. 2019

Int J Oncol

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The assessment of the risk of biochemical recurrence (BCR) is critical in the management of males with prostate cancer (PC). Over the past decades, a comprehensive effort has been focusing on improving risk stratification; a variety of models have been constructed using PC-associated pathological features and molecular alterations occurring at the genome, protein and RNA level. Alterations in RNA expression (lncRNA, miRNA and mRNA) constitute the largest proportion of the biomarkers of BCR. In this article, we systemically review RNA-based BCR biomarkers reported in PubMed according to the PRISMA guidelines. Individual miRNAs, mRNAs, lncRNAs and multigene panels, including the commercially available signatures, Oncotype DX and Prolaris, will be discussed; details related to cohort size, hazard ratio and 95% confidence intervals will be provided. Mechanistically, these individual biomarkers affect multiple pathways critical to tumorigenesis and progression, including epithelial-mesenchymal transition (EMT), phosphatase and tensin homolog (PTEN), Wnt, growth factor receptor, cell proliferation, immune checkpoints and others. This variety in the mechanisms involved not only validates their associations with BCR, but also highlights the need for the coverage of multiple pathways in order to effectively stratify the risk of BCR. Updates of novel biomarkers and their mechanistic insights are considered, which suggests new avenues to pursue in the prediction of BCR. Additionally, the management of patients with BCR and the potential utility of the stratification of the risk of BCR in salvage treatment decision making for these patients are briefly covered. Limitations will also be discussed. Contents 1. Introduction 2. Stratification of BCR risk: An update 3. Searching methods for RNA-based BCR biomarkers 4. Gene expression-based biomarkers 5. Management of patients with biochemical recurrence 6. Perspectives

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“…11 Mechanistically, lncRNAs form regulatory networks with miRNAs and mRNAs or associate with RNA bind proteins to modulate their function. 12,13 Recent studies demonstrated that some lncRNAs participate in sorafenib resistance. For example, depletion of endogenous lncRNA TUC338 can target RASAL1 3ʹ-UTR and activate the RASAL1 pathway, which sensitizes HCC cells to the treatment of sorafenib.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA DANCR Promotes Sorafenib Resistance via Activation of IL-6/STAT3 Signaling in Hepatocellular Carcinoma Cells</p>

Liu¹,

Chen²,

Yuan³

et al. 2020

OTT

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Background: Hepatocellular carcinoma (HCC) is one of the major malignancies and the second most common cause of cancer-related death worldwide. Sorafenib, an approved first-line systematic treatment agent for HCC, is capable to effectively improve the survival of patients with advanced HCC. The long-noncoding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) has been reported to exert oncogenic functions in several kinds of human cancers. However, the role of lncRNA DANCR in sorafenib resistance in HCC remains unknown. Methods: The expression levels of DANCR in HCC tissues were detected by qRT-PCR. DANCR overexpression and knockdown models were established and utilized to investigate the functional role of DANCR on sorafenib resistance in HCC cells. The MS2-binding sequences-MS2-binding protein-based RNA immunoprecipitation assay, RNA pull-down and luciferase reporter assay was used to detect the association between DANCR and PSMD10 mRNA. The activation of DANCR transcription mediated by STAT3 was assessed by luciferase reporter and chromatin immunoprecipitation assays. Results: We found that DANCR was significantly overexpressed in HCC tissues and associated with prognosis of HCC patients. Overexpression and knockdown experiments demonstrated that DANCR promoted sorafenib resistance in HCC cells in vitro and in vivo. Mechanistically, the role of DANCR relied largely on the association with PSMD10. DANCR stabilized PSMD10 mRNA through blocking the repressing effect of several microRNAs on PSMD10. Besides, DANCR activated IL-6/STAT3 signaling via PSMD10. Furthermore, we revealed that DANCR transcription was enhanced by the activation of IL-6/ STAT3 signaling, indicating a positive feedback loop of DANCR and IL-6/STAT3 signaling. Conclusion: Collectively, our study is the first to elucidate the mechanism of DANCRmediated sorafenib resistance via PSMD10-IL-6/STAT3 signaling axis, which provides a promising target for developing new therapeutic strategy for sorafenib tolerance of HCC.

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Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Cited by 37 publications

References 141 publications

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Assessment of biochemical recurrence of prostate cancer (Review)

<p>LncRNA DANCR Promotes Sorafenib Resistance via Activation of IL-6/STAT3 Signaling in Hepatocellular Carcinoma Cells</p>

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