NUCKS1 Promotes Proliferation, Invasion and Migration of Non-Small Cell Lung Cancer by Upregulating CDK1 Expression

Zhao, Shufen; Wang, Baiyao; Ma, Yanning; Kuang, Junjie; Liang, Jiyun; Yang, Yuan

doi:10.2147/cmar.s282181

Cited by 25 publications

(25 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 39 Furthermore, NUCKS1 elevation interacted with CDK1, thereby accelerating tumor growth in NSCLC. 23 Herein, NUCKS1 was upregulated in NSCLC, and NUCKS1 upregulation offset the inhibiting impact of miR‐433‐3p elevation on NSCLC cell proliferation, migration, invasion, and the Warburg effect. Importantly, circ_0008037 could regulate NUCKS1 expression by adsorbing miR‐433‐3p.…”

Section: Discussionmentioning

confidence: 84%

See 1 more Smart Citation

CircRNA circ_0008037 facilitates tumor growth and the Warburg effect via upregulating NUCKS1 by binding to miR‐433‐3p in non‐small cell lung cancer

Zhang

Zhao

et al. 2021

Thoracic Cancer

View full text Add to dashboard Cite

Background: Circular RNAs (circRNAs) participate in the genesis and progression of tumors, including non-small cell lung cancer (NSCLC). At present, the role and regulatory mechanisms of circRNAs in NSCLC have not been fully elucidated. The aim of this study was to explore the role and regulatory mechanism of circRNA hsa_circ_0008037 (circ_0008037) in NSCLC. Methods: Expression of circ_0008037 in NSCLC tissues and cells was detected by quantitative real-time polymerase chain reaction (RT-qPCR). Loss-of-function experiments were performed to analyze the influence of circ_0008037 knockdown on proliferation, migration, invasion, and the Warburg effect of NSCLC cells. Western blotting was utilized for protein analysis. The regulatory mechanism of circ_0008037 was surveyed by bioinformatics analysis, RNA pulldown assay, and dual-luciferase reporter assay. Xenograft assay was used to validate the oncogenicity of circ_0008037 in NSCLC in vivo. Results: Circ_0008037 was upregulated in NSCLC tissues and cells. Circ_0008037 downregulation reduced tumor growth in vivo and repressed proliferation, migration, invasion, and decreased the Warburg effect of NSCLC cells in vitro. Mechanically, circ_0008037 regulated nuclear ubiquitous casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) expression via sponging miR-433-3p. Furthermore, MiR-433-3p inhibitor reversed the inhibiting influence of circ_0008037 silencing on proliferation, migration, invasion, and the Warburg effect of NSCLC cells. Also, NUCKS1 elevation overturned the repressive influence of miR-433-3p mimic on proliferation, migration, invasion, and the Warburg effect of NSCLC cells. Conclusion: Circ_0008037 accelerated tumor growth and elevated the Warburg effect via regulating NUCKS1 expression by adsorbing miR-433-3p, providing an underlying target for NSCLC treatment. K E Y W O R D S circ_0008037, miR-433-3p, NSCLC, NUCKS1 † Jia Yu and Haining Zhang contribute to this work equally as co-first authors.

show abstract

Section: Discussionmentioning

confidence: 84%

“… 20 Recent studies have revealed that NUCKS1 act as an oncogene in gastric cancer, 21 hepatocellular carcinoma, 22 and NSCLC. 23 However, the regulatory network related to NUCKS1 in NSCLC is still indistinct.…”

Section: Introductionmentioning

confidence: 99%

CircRNA circ_0008037 facilitates tumor growth and the Warburg effect via upregulating NUCKS1 by binding to miR‐433‐3p in non‐small cell lung cancer

Zhang

Zhao

et al. 2021

Thoracic Cancer

View full text Add to dashboard Cite

show abstract

“…CDK1 is mainly responsible for promoting G1/S phase and G2/M switching (14). Previous studies have also shown that CDK1 is abnormally expressed in a variety of tumors (15,16). Based on the GSEA method, the relationship between the expression level of CDK1 in the RB tissues and the cell cycle was analyzed.…”

Section: Discussionmentioning

confidence: 99%

Exploration of retinoblastoma pathogenesis with bioinformatics

Zhang¹,

Zhou²,

Wang³

et al. 2021

Transl Cancer Res TCR

View full text Add to dashboard Cite

Background: Differentially expressed genes (DEGs) from retinoblastoma (RB) tissues play key roles in the progression of RB. However, the role of DEGs in different subtypes and stages of RB has not yet been systematically analyzed.Methods: In this study, the DEGs for tumor and adjacent from 3 RB data sets GSE24673, GSE97508, and GSE110811 were analyzed with regard to the different subtypes and stages of the disease.Results: Through comparison with adjacent tissues, a total of 78 upregulated genes and 155 downregulated genes from the RB tissues were identified across the 3 data sets. Gene set enrichment analysis (GSEA) showed that the 3 representative genes CDK1, CDC20, and BUB1, which were all upregulated, could promote the cell cycle in RB. Compared with adjacent tissues in GSE97508, a total of 19 gigantol-targeted genes were predicted to be upregulated in invasive RB tissues. On the other hand, DEGs for tumor and adjacent from 3 RB data sets GSE24673, GSE97508, and GSE110811 were integrated with regard to invasiveness and stages of the disease, and another 19 DEGs were subsequently identified. Among these genes, UHRF1 was the only identified upregulated gene, while the other 18 were all downregulated genes. Cell Counting Kit-8 (CCK-8) experiment and GSEA results showed that UHRF1 can promote the proliferation and invasion of RB.Conversely, the downregulated representative gene CADM1 is a tumor suppressor gene, which can inhibit the progression of RB.Conclusions: This study indicated that the verified DEGs are continuously and consistently expressed in different subtypes and stages of RB. These DEGs may be the key to understanding the development and invasion of RB.

show abstract

“…NUCKS1 also exhibits oncogenic properties, and its overexpression, correlating with poor patient prognosis, has been reported in a number of cancers 33 – 38 . Furthermore, NUCKS1 depletion inhibits—while its overexpression promotes—xenograft tumour growth 18 , 39 , 40 , suggesting a direct role in tumourigenesis.…”

Section: Introductionmentioning

confidence: 99%

The NUCKS1-SKP2-p21/p27 axis controls S phase entry

et al. 2021

View full text Add to dashboard Cite

Efficient entry into S phase of the cell cycle is necessary for embryonic development and tissue homoeostasis. However, unscheduled S phase entry triggers DNA damage and promotes oncogenesis, underlining the requirement for strict control. Here, we identify the NUCKS1-SKP2-p21/p27 axis as a checkpoint pathway for the G1/S transition. In response to mitogenic stimulation, NUCKS1, a transcription factor, is recruited to chromatin to activate expression of SKP2, the F-box component of the SCFSKP2 ubiquitin ligase, leading to degradation of p21 and p27 and promoting progression into S phase. In contrast, DNA damage induces p53-dependent transcriptional repression of NUCKS1, leading to SKP2 downregulation, p21/p27 upregulation, and cell cycle arrest. We propose that the NUCKS1-SKP2-p21/p27 axis integrates mitogenic and DNA damage signalling to control S phase entry. The Cancer Genome Atlas (TCGA) data reveal that this mechanism is hijacked in many cancers, potentially allowing cancer cells to sustain uncontrolled proliferation.

show abstract

NUCKS1 Promotes Proliferation, Invasion and Migration of Non-Small Cell Lung Cancer by Upregulating CDK1 Expression

Cited by 25 publications

References 31 publications

CircRNA circ_0008037 facilitates tumor growth and the Warburg effect via upregulating NUCKS1 by binding to miR‐433‐3p in non‐small cell lung cancer

CircRNA circ_0008037 facilitates tumor growth and the Warburg effect via upregulating NUCKS1 by binding to miR‐433‐3p in non‐small cell lung cancer

Exploration of retinoblastoma pathogenesis with bioinformatics

The NUCKS1-SKP2-p21/p27 axis controls S phase entry

Contact Info

Product

Resources

About