LncRNA UCA1 promotes the invasion and EMT of bladder cancer cells by regulating the miR‑143/HMGB1 pathway

Luo, Junpeng; Chen, Jing; Li, Hang; Yu, Yang; Yun, Haichao; Yang, Shangqi; Mao, Xiangming

doi:10.3892/ol.2017.6886

Cited by 61 publications

(69 citation statements)

References 50 publications

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“…18,19 However, little study has investigated the regulatory effect of mRNA on lncRNA through sponging miRNA. 9 According to these evidence, the upregulation of lncRNA-UCA1 as the result of SATB1/miR-495-3p interplay network is likely an importance mechanism underlying GC proliferation and progression. The upregulation of SATB1 in GC, thus, more likely increased lncRNA-UCA1 expression.…”

Section: Discussionmentioning

confidence: 97%

“…[3][4][5] The regulatory effects of SATB1 on the metastasis and multidrug resistance of GC have been regarded as major mechanisms underlying the poor prognosis. [7][8][9][10][11][12] As increased lncRNA-UCA1 is associated with poor overall survival and disease-free survival of GC patients, lncRNA-UCA1 has been suggested as a promising biomarker for the early detection and prognosis prediction. Increasing studies is going to unravel the molecular basis by which SATB1 regulates the proliferation, invasion, and multidrug resistance of GC cells.…”

Section: Introductionmentioning

confidence: 99%

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SATB1 3′‐UTR and lncRNA‐UCA1 competitively bind to miR‐495‐3p and together regulate the proliferation and invasion of gastric cancer

Sun

Liu

Yang

et al. 2018

J of Cellular Biochemistry

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High expression of special AT‐rich‐binding protein 1 (SATB1) correlates with the advanced TNM stage and short overall and recurrence‐free survival of gastric cancer (GC). A bioinformatic analysis revealed that SATB1 3′‐untranslated region (3′‐UTR) and long noncoding RNA UCA1 (lncRNA‐UCA1) might competitively bind to microRNA‐495‐3p (miR‐495‐3p). Interestingly, lncRNA‐UCA1 is also an important contributor to GC. The current study aimed to demonstrate the potential interaction among SATB1/miR‐495‐3p/lncRNA‐UCA1 network and their effects on GC proliferation and invasion. The expression in GC and paracancerous normal tissues were assessed using real‐time polymerase chain reaction and Western blot analysis. Luciferase reporter, RNA pull‐down, and transfection assays were performed to determine the interaction among SATB1/miR‐495‐3p/lncRNA‐UCA1 network in GC cells. GC proliferation and invasion were evaluated using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide, transwell invasion, and colony formation assays. Results showed higher expression of SATB1 and lncRNA‐UCA1 but lower miR‐495‐3p expression in GC than in the normal tissues. In luciferase reporter assay, miR‐495‐3p bound to three seed sequences in SATB1 3′‐UTR but only one in lncRNA‐UCA1. SATB1 knockdown increased the combination of miR‐495‐3p with lncRNA‐UCA1 but decreased lncRNA‐UCA1 expression. Decreased lncRNA‐UCA1 was also observed with the mimics increased miR‐495‐3p. These data suggested that SATB1 3′‐UTR functions as a competing endogenous RNA of miR‐495‐3p and positively regulates lncRNA‐UCA1. LncRNA‐UCA1 knockdown only decreased SATB1 expression in MKN‐45 cells but not in BGC‐823 cells, which suggested that the regulatory effect of lncRNA‐UCA1 on SATB1 by sponging miR‐495‐3p is cell‐dependent. This study further identified that SATB1/miR‐495‐3p/lncRNA‐UCA1 network is implicated in GC proliferation and invasion. The current study firstly revealed that SATB1 interacts with miR‐495‐3p/lncRNA‐UCA1 network, whereby enhancing GC proliferation and invasion.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

SATB1 3′‐UTR and lncRNA‐UCA1 competitively bind to miR‐495‐3p and together regulate the proliferation and invasion of gastric cancer

Sun

Liu

Yang

et al. 2018

J of Cellular Biochemistry

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“…UCA1 overexpression in bladder cancer significantly repressed miR-143 expression [95]. MiR-143 exerted a tumor suppressive role by targeting the 3 0 UTR of HMGB1, leading to the up-regulation of EMT, which was associated with invasion of bladder cancer [95]. Similarly, UCA1 up-regulated EMT and promoted the invasion of bladder cancer cells though targeting the miR-145-ZEB1/2-fascin homologue 1 pathway [96].…”

Section: Bladder Cancermentioning

confidence: 99%

“…Bladder cancer is a highly prevalent disease with substantial morbidity and mortality [94]. UCA1 overexpression in bladder cancer significantly repressed miR-143 expression [95]. MiR-143 exerted a tumor suppressive role by targeting the 3 0 UTR of HMGB1, leading to the up-regulation of EMT, which was associated with invasion of bladder cancer [95].…”

Section: Bladder Cancermentioning

confidence: 99%

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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“…UCA1 is a potential new oncogene and prognostic factor in kinds of cancers. For example, UCA1 was regarded as an oncogenic lncRNA in bladder cancer, and up-regulated UCA1 is associated with enhanced cell invasion [17]. Besides, UCA1 was found to be up-regulated in colorectal cancer and UCA1 level is negatively correlated with survival time [18].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA UCA1 exerts growth modulation by miR-15a in human thyroid cancer TPC-1 cells

Hao

Zhang

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Thyroid cancer is widely diagnosed as malignancy in endocrine system. This study attempted to validate UCA1 possessed modulatory function on cell proliferation and epithelial mesenchymal transition (EMT) in human thyroid cancer cell line TPC-1. Ectopic expression of UCA1 was induced in TPC-1 cells by transfection. CCK-8 assays were employed to value cell viability. Cell apoptosis analysis was conducted through flow cytometry. We found that overexpressed UCA1 strongly promoted cell proliferation. However, the knockdown of UCA1 suppressed cell proliferation and induced obvious cell apoptosis. Besides, cell EMT was promoted by overexpressed UCA1 and was inhibited by the knockdown of UCA1. Further study revealed that miR-15a level in TPC-1 cells was suppressed by overexpressed UCA1. Simultaneous overexpression of UCA1 and miR-15a partly alleviated UCA1-induced growth, identifying that miR-15a was a possible target of UCA1. At last, the Hippo and JNK signal pathways were activated by overexpressed UCA1 but were then weakened by the adding of miR-15a. In conclusion, our study revealed UCA1/miR-15a axis implicated in thyroid cancer cells EMT, exposing a novel mechanism of thyroid cancer progression. ARTICLE HISTORY

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LncRNA UCA1 promotes the invasion and EMT of bladder cancer cells by regulating the miR‑143/HMGB1 pathway

Cited by 61 publications

References 50 publications

SATB1 3′‐UTR and lncRNA‐UCA1 competitively bind to miR‐495‐3p and together regulate the proliferation and invasion of gastric cancer

SATB1 3′‐UTR and lncRNA‐UCA1 competitively bind to miR‐495‐3p and together regulate the proliferation and invasion of gastric cancer

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Long non-coding RNA UCA1 exerts growth modulation by miR-15a in human thyroid cancer TPC-1 cells

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