LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495

Lü, Yun; Liu, Weigang; Lü, Jiahui; Liu, Zhi Jun; Li, Haibin; Liu, Gui-Jing; She, Hongyan; Li, Guiying; Shi, Xin-Hua

doi:10.1177/1010428317701632

Cited by 35 publications

(21 citation statements)

References 28 publications

(36 reference statements)

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“…Consistently, miR129-3p weakened migration and invasion of RCC cells [104], while SOX4 facilitated migration of RCC cells [105]. In addition, UCA1 promoted proliferation of RCC through sponging miR-495, whose downstream target is EZH2 [106].…”

Section: Renal Cell Carcinomamentioning

confidence: 77%

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

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Long non-coding RNAs (lncRNAs) are a major subset of highly conserved non-coding RNAs (ncRNAs) that consist of at least 200 nucleotides and have limited protein-coding potential. Cumulative data have shown that lncRNAs are deregulated in many types of cancer and may control pathophysiological processes of cancer at various levels, including transcription, post-transcription and translation. Recently, lncRNAs have been demonstrated to interact with microRNAs (miRNAs), another major subset of ncRNAs, which regulate physiological and pathological processes by inhibiting target mRNA translation or promoting mRNA degradation. The lncRNA urothelial carcinomaassociated 1 (UCA1) has recently gained much attention as it is overexpressed in many types of cancer and is involved in carcinogenesis. Here, we review the crosstalk between UCA1 and miRNAs during the pathogenesis of cancer, with a focus on cancer-cell proliferation, invasion, drug resistance, and metabolism.

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Section: Renal Cell Carcinomamentioning

confidence: 77%

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

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“…Furthermore, UCA1 impacts the activation of CREB and AKT, and contributes to tamoxifen resistance via PI3K/AKT-dependent signaling in human breast cancer. UCA1, urothelial cancer associated 1; PI3K, phosphoinositide 3-kinase; EZH2, enhancer of zeste homolog 2. by UCA1 in renal cell carcinoma cells (40). EZH2 is a histone methyltransferase that catalyzes the trimethylation of H3K27me3 of target genes.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA UCA1 confers tamoxifen resistance in breast cancer endocrinotherapy through regulation of the EZH2/p21 axis and the PI3K/AKT signaling pathway

et al. 2019

Int J Oncol

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Tamoxifen is the gold standard for breast cancer endocrinotherapy. However, drug resistance remains a major limiting factor of tamoxifen treatment. Long non-coding (lnc) RNA serves an important role in drug resistance; however, the molecular mechanisms of tamoxifen resistance in breast cancer endocrinotherapy are largely unclear. lncRNA urothelial cancer associated 1 (lncRNA UCA1, UCA1) has been proven to be dysregulated in human breast cancer and promotes cancer progression. In the present study, it was demonstrated that UCA1 was significantly upregulated in breast cancer tissues compared with healthy tissues. Furthermore, the expression level of UCA1 was significantly greater in tamoxifen-resistant breast cancer cells (LCC2 and LCC9) when compared with those in the tamoxifen-sensitive breast cancer cells (MCF-7 and T47D). UCA1 silencing in LLC2 and LLC9 cells increased tamoxifen drug sensitivity by promoting cell apoptosis and arresting the cell cycle at the G 2 /M phase. Notably, the induced overexpression of UCA1 in MCF-7 and T47D cells decreased the drug sensitivity of tamoxifen. The molecular mechanism involved in UCA1-induced tamoxifen-resistance was also investigated. It was identified that UCA1 was physically associated with the enhancer of zeste homolog 2 (EZH2), which suppressed the expression of p21 through histone methylation (H3K27me3) on the p21 promoter. In addition, it was demonstrated that UCA1 expression was paralleled to the phosphorylation of CAMP responsive element binding protein (CREB) and AKT. When LCC2 cells were treated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway inhibitor LY294002, the phosphorylation levels of CREB and AKT were significantly downregulated. Taken together, it was concluded that UCA1 regulates the EZH2/p21 axis and the PI3K/AKT signaling pathway in breast cancer, and may be a potential therapeutic target for solving tamoxifen resistance.

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“…For example, the lncRNA GAS5 suppresses cell growth and epithelial‐mesenchymal transition in osteosarcoma through repressing the miR‐221/ARHI Pathway (Ye et al, ). LncRNA UCA1 can promote renal cell carcinoma proliferation via epigenetically repressing p21 expression and negatively regulating miR‐495 (Lu et al, ). For another, microRNA‐26a inhibits proliferation and metastasis of human hepatocellular carcinoma by regulating DNMT3B‐MEG3 axis (Li et al, ).…”

Section: Discussionmentioning

confidence: 99%

LncRNA DGCR5 promotes lung adenocarcinoma (LUAD) progression via inhibiting hsa‐mir‐22‐3p

Dong

Ren

Jin

et al. 2017

Journal Cellular Physiology

139

135

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Long non-coding RNAs (lncRNAs) serve critical roles in the pathogenesis of various cancers, including lung adenocarcinoma (LUAD). Herein, in this study, we aimed to investigate the biological and clinical significance of lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) in LUAD. It was observed that DGCR5 was upregulated in LUAD tissues and LUAD cell lines. Inhibition of DGCR5 can prevent LUAD progression via playing anti-apoptosis roles. Both mRNA expression and protein levels of BCL-2 were increased by DGCR5 downregulation while reversely BAX was increased. Additionally, a novel microRNA target of DGCR5, hsa-mir-22-3p was identified through bioinformatics search and confirmed by dual-luciferase reporter system. Gain and loss-of-function studies were performed to verify whether DGCR5 exerts its biological functions through regulating hsa-mir-22-3p in vitro. Overexpression of DGCR5 was able to reverse the tumor inhibitory effect of hsa-mir-22-3p mimics. Furthermore, in vivo tests tumor xenografts were established to detect the function of DGCR5 in LUAD tumorigenesis. Downregulated DGCR5 expression was greatly associated with smaller tumor size, implying a favorable prognosis of LUAD patients. Taken these together, DGCR5 could be considered as a prognostic biomarker and therapeutic target in LUAD diagnosis and treatment.

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LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495

Cited by 35 publications

References 28 publications

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Long non‑coding RNA UCA1 confers tamoxifen resistance in breast cancer endocrinotherapy through regulation of the EZH2/p21 axis and the PI3K/AKT signaling pathway

LncRNA DGCR5 promotes lung adenocarcinoma (LUAD) progression via inhibiting hsa‐mir‐22‐3p

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