<i>Retracted:</i> LncRNA UCA1 impacts cell proliferation, invasion, and migration of pancreatic cancer through regulating miR‐96/<i>FOXO3</i>

Zhou, Yalu; Chen, Yigang; Ding, Wenzhou; Hua, Zhiyuan; Wang, Liying; Zhu, Ye; Qian, Haixin; Dai, Tu

doi:10.1002/iub.1699

Cited by 71 publications

(54 citation statements)

References 32 publications

(40 reference statements)

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“…UCA1 promoted migration of pancreatic cancer by sponging miR-107 targeting integrin subunit a 2 (ITGA2) [74]. FOXO3, a target of miR-96, could impair pancreatic cancer cell viability and inhibit cell apoptosis [75]. FOXO3, a target of miR-96, could impair pancreatic cancer cell viability and inhibit cell apoptosis [75].…”

Section: Pancreatic Cancermentioning

confidence: 99%

“…Moreover, UCA1 could promote pancreatic cancer cell multiplication and metastatic ability by down-regulating miR-96 and up-regulating forkhead box O3 (FOXO3). FOXO3, a target of miR-96, could impair pancreatic cancer cell viability and inhibit cell apoptosis [75]. Furthermore, UCA1 promoted growth and metastasis of pancreatic cancer by sponging miR-135a [76].…”

Section: Pancreatic Cancermentioning

confidence: 99%

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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: Pancreatic Cancermentioning

confidence: 99%

Section: Pancreatic Cancermentioning

confidence: 99%

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

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“…[7][8][9] Originally, NF-κB interacting lncRNA (NKILA) was found to be as a lncRNA mediated by NF-κB signaling pathway inducing inflammatory cytokines such as TNF-α and IL-1β in breast cancer cell. [7][8][9] Originally, NF-κB interacting lncRNA (NKILA) was found to be as a lncRNA mediated by NF-κB signaling pathway inducing inflammatory cytokines such as TNF-α and IL-1β in breast cancer cell.…”

Section: Introductionmentioning

confidence: 99%

LncRNA NKILA correlates with the malignant status and serves as a tumor‐suppressive role in rectal cancer

Tao

Yang

et al. 2018

J of Cellular Biochemistry

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NF-κB interacting lncRNA (NKILA) has been found to function as a tumor-suppressive role in various human cancers. However, the role of NKILA in rectal cancer is still unknown. The objective of this study is to investigate the clinical value and biological function of NKILA in rectal cancer. The association between NKILA expression and clinical variables including prognosis was estimated in rectal cancer patients. The gain-of-function study of NKILA in rectal cancer cell was conducted to evaluate the effect of NKILA on cell proliferation, migration, invasion, and NF-κB signaling pathway. The results suggested NKILA expression was decreased in rectal cancer tissues and cells, and correlated with clinical stage, T classification, N classification and M classification. NKILA low-expression was an independent poor prognostic factor in rectal cancer patients. NKILA-inhibited rectal cancer cell proliferation, migration, and invasion via suppressing NF-κB signaling. In conclusion, NKILA serves as an antioncogenic lncRNA in rectal cancer.

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“…[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%

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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Retracted: LncRNA UCA1 impacts cell proliferation, invasion, and migration of pancreatic cancer through regulating miR‐96/FOXO3

Cited by 71 publications

References 32 publications

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

LncRNA NKILA correlates with the malignant status and serves as a tumor‐suppressive role in rectal cancer

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

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