Knockdown of CREB1 inhibits tumor growth of human gastric cancer in vitro and in vivo

Rao, Min; Zhu, Yao; Cong, Xiaoxia; Li, Qianxun

doi:10.3892/or.2017.5636

Cited by 46 publications

(42 citation statements)

References 26 publications

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“…A previous report has indicated that CREB1 acts as an oncogene in GC; specifically, miRNA-122 inhibits proliferation and invasion in gastric cancer by targeting CREB1 [24]. Knockdown of CREB1 inhibits tumor growth of human gastric cancer in vitro and in vivo [25]. In the current study, using predictive tools and luciferase reporter gene assay analysis, we demonstrated that CREB1 is a target of miR-590-3p in GC cells.…”

Section: Discussionsupporting

confidence: 57%

UCA1 promotes cell proliferation and invasion of gastric cancer by targeting CREB1 sponging to miR‐590‐3p

Lü

Zhou

et al. 2018

Cancer Medicine

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Long noncoding RNAs (lncRNAs) have emerged as regulators in a variety of biological processes, including carcinogenesis in human cancer. UCA1 has been reported to be upregulated in gastric cancer (GC); however, the underlying functional roles of UCA1 in GC have not been established. In the current study, we showed that UCA1 is significantly higher in GC tissues and cells compared with adjacent normal tissues and a gastric epithelium cell line, respectively. Higher UCA1 expression was associated with lymph node metastasis, TNM stage, and poor overall survival (OS) in GC patients. In vitro functional studies confirmed that UCA1 promotes cell proliferation, colony formation ability, and cell invasion in GC cells. We demonstrated that knockdown of UCA1 inhibits tumor growth in vivo. The double luciferase reporter, RNA‐binding protein immunoprecipitation assay, and RNA pull down assay demonstrated that miR‐590‐3p serves as a target for UCA1. UCA1 promoted cell proliferation and invasion by negatively regulating miR‐590‐3p expression. Moreover, we demonstrated that CREB1 is a downstream target of miR‐590‐3p and UCA1 activates CREB1 expression by sponging to miR‐590‐3p. Thus, these results showed that UCA1 functions as an oncogene in GC and may be a target for treatment of GC.

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Section: Discussionsupporting

confidence: 57%

UCA1 promotes cell proliferation and invasion of gastric cancer by targeting CREB1 sponging to miR‐590‐3p

Lü

Zhou

et al. 2018

Cancer Medicine

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“…Analogously, studies have reported that inositol-6 phosphate (IP-6) and lncRNA UBE2CP3-001 inhibit apoptosis in some cancers [29,30]. Furthermore, CREB1 overexpression is associated with increased cell proliferation and decreased apoptotic sensitivity [31,32]. In our study, cell viability was increased and apoptosis was decreased when CREB1 was overexpressed in the RB cell model, which is consistent with the findings from Qian et al on malignant glioma cells [26].…”

Section: Discussionsupporting

confidence: 92%

“…Zhang et al reported that CREB1-induced histone H3 acetylation facilitates the transition of G0 to S phase cells in prostate cancer [34]. In addition, CREB1 has been reported to be able bind to the promoters of cell cycle genes, including cyclin A, B1, D1, D2 and Wnt10b and regulates the transcription of these genes, thereby regulating cell proliferation [31,35]. Similarly, this study revealed that miR-133a-3p prevented the transition from G1 to S phase in Y97 cells, causing cell cycle arrest and down-regulation of cyclin B1 and D1.…”

Section: Discussionmentioning

confidence: 99%

miR-133a-3p promotes apoptosis and induces cell cycle arrest by targeting CREB1 in retinoblastoma

Liu

Wang

et al. 2020

aoms

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Introduction: Retinoblastoma (RB) is a malignant tumor that is derived from photoreceptors. It is common in children under 3 years old with a family genetic predisposition. MicroRNA-133a-3p (miR-133a-3p) is one of the tumor-related miRNAs that interprets a critical function in the genesis and development of various tumors. This study investigated the effects and underlying mechanisms of miR-133a-3p in RB. Material and methods: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis was used to assess the miR-133a-3p expression in RB tissues and a cell model. MTT assay, western blot, flow cytometry and luciferase reporter assay were performed to evaluate the effect of miR-133a-3p on cell viability, apoptosis and the cell cycle. An RB xenograft model was established to assess the in vivo influence of miR-133a-3p on RB growth. Results: MiR-133a-3p level was reduced in RB tissues and the cell model (p < 0.01 or p < 0.001). Addition of miR-133a-3p reduced cell viability, and increased apoptosis and cell cycle arrest (p < 0.001). Additionally, CREB1 was identified to be the target of miR-133a-3p in RB cell lines (p < 0.001). Cell viability reduction, apoptosis and cell cycle arrest increases mediated by miR-133a-3p were attenuated by CREB1 overexpression (p < 0.001). MiR-133a-3p inhibited tumor growth of RB in vivo (p < 0.001). Conclusions: Our results reveal that miR-133a-3p exhibits anti-cancer effects by targeting CREB1 in RB. This study provides a new direction for effective targeted treatment of this disease.

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“…SATB1 is a target of miR-495-3p and positively correlated with the advanced tumor node metastasis stage of GC [66]. Furthermore, UCA1 could sponge the miR-590-3p targeting cyclic adenosine monophosphate response element-binding protein 1 (CREB1), and knockdown of CREB1 inhibits the growth of human GC in vitro and in vivo [67,68]. Moreover, UCA1 increased multi-drug resistance of GC by downregulating miR-27b [69].…”

Section: Gastrointestinal Cancersmentioning

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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Knockdown of CREB1 inhibits tumor growth of human gastric cancer in vitro and in vivo

Cited by 46 publications

References 26 publications

UCA1 promotes cell proliferation and invasion of gastric cancer by targeting CREB1 sponging to miR‐590‐3p

UCA1 promotes cell proliferation and invasion of gastric cancer by targeting CREB1 sponging to miR‐590‐3p

miR-133a-3p promotes apoptosis and induces cell cycle arrest by targeting CREB1 in retinoblastoma

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

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