CircNR3C1 inhibits proliferation of bladder cancer cells by sponging miR-27a-3p and downregulating cyclin D1 expression

Zheng, Fuxin; Wang, Miao; Li, Yawei; Huang, Chao; Tang, Dan; Xie, Fei; Zhang, Hui; Sun, Jiayin; Zhang, Chuanhua; Li, Zhuoshi; Wang, Zhendi; Jiang, Guosong

doi:10.1016/j.canlet.2019.06.018

Cited by 64 publications

(41 citation statements)

References 50 publications

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“…Results showed that DJ-1 activated cyclin-D1 and MDM2-p53 signaling, which modulate CRC pathogenesis and progression. A previous study reported that DJ-1 induced G1 arrest by decreasing cyclin-E1 in HCT8 cells (28). The results indicated that DJ-1 triggered G1-S phase arrest in HCT116 and SW480 cells ( Figure 5, A-H).…”

Section: Discussionmentioning

confidence: 66%

Overexpression of DJ-1 enhances colorectal cancer cell proliferation through the cyclin-D1/MDM2-p53 signaling pathway

Zhu

Luo

Kang

et al. 2020

BST

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Emerging evidence indicates that DJ-1 is highly expressed in different cancers. It modulates cancer progression, including cell proliferation, cell apoptosis, invasion, and metastasis. However, its role in colorectal cancer (CRC) remains poorly defined. The current study noted increased DJ-1 expression in CRC tumor tissue and found that its expression was closely related to clinicalpathological features. Similarly, DJ-1 increased in CRC cells (SW480, HT-29, Caco-2, LoVo, HCT116, and SW620), and especially in SW480 and HCT116 cells. Functional analyses indicated that overexpression of DJ-1 promoted CRC cell invasion, migration, and proliferation in vitro and in vivo. Mechanistic studies indicated that DJ-1 increased in CRC cell lines, activated specific protein cyclin-D1, and modulated the MDM2/p53 signaling pathway by regulating the levels of the downstream factors Bax, Caspase-3, and Bcl-2, which are related to the cell cycle and apoptosis. Conversely, knockdown of DJ-1 upregulated p53 expression by disrupting the interaction between p53 and MDM2 and inhibiting CRC cell proliferation, revealing the pro-oncogenic mechanism of DJ-1 in CRC. In conclusion, the current findings provide compelling evidence that DJ-1 might be a promoter of CRC cell invasion, proliferation, and migration via the cyclin-D1/MDM2-p53 signaling pathway. Findings also suggest its potential role as a postoperative adjuvant therapy for patients with CRC.

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Section: Discussionmentioning

confidence: 66%

Overexpression of DJ-1 enhances colorectal cancer cell proliferation through the cyclin-D1/MDM2-p53 signaling pathway

Zhu

Luo

Kang

et al. 2020

BST

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“…First, we performed in vitro experi- variety of human cancers, including BC. [25][26][27][28][29] We therefore predicted that these proteins may be useful markers to monitor biological behaviours of BC cells in SNHG1-mediated modulation. Collectively, these results revealed that SNHG1 is capable of promoting BC progression by facilitating BC cell proliferation, migration, invasion and EMT.…”

Section: Snhg1 Promotes the Proliferation Migration And Invasion Omentioning

confidence: 99%

The long non‐coding RNA SNHG1 promotes bladder cancer progression by interacting with miR‐143‐3p and EZH2

Wei

Lyu

Huang

et al. 2020

J Cellular Molecular Medi

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Bladder cancer (BC), one of the most lethal neoplasms of the genitourinary system worldwide, has shown a trend towards increasing incidence and mortality rates in recent years. 1 Despite substantial progress in understanding the pathophysiology of BC, the exact mechanisms underlying bladder carcinogenesis remain unclear. Therefore, identifying novel molecular targets and more effective therapeutic approaches is of crucial importance to improve the treatment and prognosis of BC. Currently, emerging evidence has indicated that non-coding RNAs (ncRNAs) are involved in the pathogenesis of human carcinomas, providing novel insights into mechanistic research on the occurrence and development of malignant neoplasms. 2 miRNAs are a group of small ncRNAs with an average length of 20-24 nucleotides that mediate the translational suppression or degradation of mRNAs by binding to their 3′-untranslated regions (3′-UTRs). 3 Additionally, lncRNAs are a subgroup of ncRNAs that have lengths greater than 200 bp. It has been generally recognized

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“…Overexpression of circNR3C1 in BC was found to reduce the expression of cyclinD1 via sponging of miR-27a-3p; a similar relationship was found between hsa_-circ_0058063, CDK6, and miR-145-5p. 95,96 Therefore, low expression of circNR3C1 and hsa_circ_0058063 in BC accelerate the G1-to-S phase transition of tumor cells and enhance cell proliferation owing to decreased sponging of their target miRNAs and subsequently increased expression of cyclinD1 and CDK6, respectively. 95,96 High expression levels of p21, a cyclindependent kinase inhibitor, can induce cell cycle arrest.…”

Section: Regulation Of the Cell Cyclementioning

confidence: 99%

<p>Circular RNAs and Bladder Cancer</p>

Cai

2020

OTT

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Bladder cancer (BC) is the most common urinary system malignancy and is a serious threat to human health. Circular RNAs (circRNAs) are members of a newly defined class of noncoding RNAs (ncRNAs) that can regulate gene expression at the transcriptional or posttranscriptional level. Studies have shown that circRNAs are related to the clinicopathological characteristics, prognosis, and chemosensitivity of BC, and basic research has further confirmed that changes in the expression of circRNAs in BC are closely related to various tumor biological functions. CircRNAs promote tumor development by interacting with miRNAs to regulate transcription factors and both classical and nonclassical tumor signaling pathways. The nonclassical signaling pathways are related to cell cycle progression, epithelial-mesenchymal transition (EMT), extracellular matrix maintenance, and tumor stem cell maintenance. In this article, the relationships between circRNAs and the clinical characteristics of BC are reviewed, and the molecular mechanisms by which circRNAs promote tumor development are explored.

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CircNR3C1 inhibits proliferation of bladder cancer cells by sponging miR-27a-3p and downregulating cyclin D1 expression

Cited by 64 publications

References 50 publications

Overexpression of DJ-1 enhances colorectal cancer cell proliferation through the cyclin-D1/MDM2-p53 signaling pathway

Overexpression of DJ-1 enhances colorectal cancer cell proliferation through the cyclin-D1/MDM2-p53 signaling pathway

The long non‐coding RNA SNHG1 promotes bladder cancer progression by interacting with miR‐143‐3p and EZH2

<p>Circular RNAs and Bladder Cancer</p>

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