NEK2 promotes esophageal squamous cell carcinoma cell proliferation, migration and invasion through the Wnt/β-catenin signaling pathway

Guo, Dong; Yao, Weinan; Du, Xuehui; Dong, Jing; Zhang, X.; Shen, Wenbin; Zhu, Shuchai

doi:10.1007/s12672-023-00692-5

Cited by 4 publications

(5 citation statements)

References 48 publications

(42 reference statements)

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“…NEK2 overexpression has been found in various human malignancies [73][74][75][76][77][78][79][80], including gastrointestinal tumors [81,82]. Aberrant NEK2 expression in cancers has been associated with tumor cell proliferation [83], migration [82], invasion [74,77], drug/radio resistance [84,85], immune response [80,86], and poor prognosis [26,75]. In our bioinformatics analyses, NEK2 is the most frequently upregulated NEK member in EAC (significantly detected in seven of the eight databases).…”

Section: Discussionmentioning

confidence: 78%

“…In addition, NEK2 may also play a role in microtubule stabilization [70], B cell development and immunological response [71], and splicing [72]. NEK2 overexpression has been found in various human malignancies [73][74][75][76][77][78][79][80], including gastrointestinal tumors [81,82]. Aberrant NEK2 expression in cancers has been associated with tumor cell proliferation [83], migration [82], invasion [74,77], drug/radio resistance [84,85], immune response [80,86], and poor prognosis [26,75].…”

Section: Discussionmentioning

confidence: 99%

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Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett’s Esophagus

Chen,

Ballout,

et al. 2023

Cancers

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The incidence of esophageal adenocarcinoma (EAC) has risen rapidly during the past four decades, making it the most common type of esophageal cancer in the USA and Western countries. The NEK (Never in mitosis A (NIMA) related kinase) gene family is a group of serine/threonine kinases with 11 members. Aberrant expression of NEKs has been recently found in a variety of human cancers and plays important roles in tumorigenesis, progression, and drug-resistance. However, the expression of the NEKs in EAC and its precancerous condition (Barrett’s esophagus, BE) has not been investigated. In the present study, we first analyzed the TCGA and 9 GEO databases (a total of 10 databases in which 8 contain EAC and 6 contain BE) using bioinformatic approaches for NEKs expression in EAC and BE. We identified that several NEK members, such as NEK2 (7/8), NEK3 (6/8), and NEK6 (6/8), were significantly upregulated in EAC as compared to normal esophagus samples. Alternatively, NEK1 was downregulated in EAC as compared to the normal esophagus. On the contrary, genomic alterations of these NEKs are not frequent in EAC. We validated the above findings using qRT-PCR and the protein expression of NEKs in EAC cell lines using Western blotting and in primary EAC tissues using immunohistochemistry and immunofluorescence. Our data suggest that frequent upregulation of NEK2, NEK3, and NEK7 may be important in EAC.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett’s Esophagus

Chen,

Ballout,

et al. 2023

Cancers

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“…Initially, NEK2's promotion of the cell cycle was identified as a major factor contributing to its pro-tumor effects. As a result, the objective of targeting NEK2 to achieve effective anti-tumor outcomes is centered around inhibiting the progression of cancer cells through slowing down their cell cycle during mitosis and cytokinesis [29,30]. NEK2 is upregulated in cancer and has been linked to the initiation, advancement, spread, and resistance to treatment of tumors [31].…”

Section: Discussionmentioning

confidence: 99%

NEK2 promotes TP53 ubiquitination to enhance the proliferation and migration of TP53 wild-type glioblastoma cells

Zhang,

Yu,

et al. 2024

neo

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The most common primary malignant tumor in the adult brain is glioblastoma multiforme (GBM); however, its underlying pathogenic mechanism remains elusive. The never in mitosis (NIMA)related kinase 2 (NEK2) has been closely associated with the prognosis of various malignancies.Nevertheless, the complete elucidation of NEK2's potential clinical value, particularly in glioma prognosis and development, remains lacking. U87MG and A172 glioblastoma cells were infected with sh-NEK2 lentivirus or oe-NEK2 plasmid to investigate the effect of NEK2 on cell proliferation, migration, and invasion. Cell viability was measured using CCK-8 and colony formation assays, while Transwell assay was utilized to assess cell migration and invasion. Protein expression levels were determined through western blot analysis. Additionally, CGGA and TCGA databases were used for bioinformatics analysis in order to examine the NEK2 expression. Through comprehensive bioinformatics analysis, we identified elevated mRNA expression levels of NEK2 in gliomas compared to normal tissues, which correlated with poor prognosis among glioma patients.Moreover, functional experiments revealed that silencing NEK2 suppressed glioma cell proliferation while overexpression of NEK2 promoted migration and invasion capabilities. Finally, our study uncovered that NEK2 regulates the malignant progression of TP53 wild-type glioblastoma by facilitating TP53 ubiquitination.

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“…Knockdown of NEK2 inhibits activation of the Wnt1/β-catenin signaling pathway [ 49 ]. The Wnt/β-catenin pathway is the downstream pathway of NEK2, which promotes cell proliferation, migration and invasion by activating the Wnt/β-catenin pathway [ 50 ]. So, the GTSE1 , MELK , CDK1 , ECT2 , and NEK2 genes may be involved in the molecular regulation of feather follicle density.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome and Weighted Gene Co-Expression Network Analysis for Feather Follicle Density in a Chinese Indigenous Breed

Wang,

Wei,

Xing

et al. 2024

Animals

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Feather follicle density plays an important role in appealing to consumers’ first impressions when making purchasing decisions. However, the molecular network that contributes to this trait remains largely unknown. The aim of this study was to perform transcriptome and weighted gene co-expression network analyses to determine the candidate genes relating to feather follicle density in Wannan male chickens. In total, five hundred one-day-old Wannan male chickens were kept in a conventional cage system. Feather follicle density was recorded for each bird at 12 weeks of age. At 12 weeks, fifteen skin tissue samples were selected for weighted gene co-expression network analysis, of which six skin tissue samples (three birds in the H group and three birds in the L group) were selected for transcriptome analysis. The results showed that, in total, 95 DEGs were identified, and 56 genes were upregulated and 39 genes were downregulated in the high-feather-follicle-density group when compared with the low-feather-follicle-density group. Thirteen co-expression gene modules were identified. The red module was highly significantly negatively correlated with feather follicle density (p < 0.01), with a significant negative correlation coefficient of −0.72. In total, 103 hub genes from the red module were screened. Upon comparing the 103 hub genes with differentially expressed genes (DEGs), it was observed that 13 genes were common to both sets, including MELK, GTSE1, CDK1, HMMR, and CENPE. From the red module, FOXM1, GTSE1, MELK, CDK1, ECT2, and NEK2 were selected as the most important genes. These genes were enriched in the DNA binding pathway, the heterocyclic compound binding pathway, the cell cycle pathway, and the oocyte meiosis pathway. This study suggests that FOXM1, GTSE1, MELK, CDK1, ECT2, and NEK2 may be involved in regulating the development of feather follicle density in Wannan male chickens. The results of this study reveal the genetic structure and molecular regulatory network of feather follicle density in Wannan male chickens, and provide a basis for further elucidating the genetic regulatory mechanism and identifying molecular markers with breeding value.

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NEK2 promotes esophageal squamous cell carcinoma cell proliferation, migration and invasion through the Wnt/β-catenin signaling pathway

Cited by 4 publications

References 48 publications

Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett’s Esophagus

Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett’s Esophagus

NEK2 promotes TP53 ubiquitination to enhance the proliferation and migration of TP53 wild-type glioblastoma cells

Transcriptome and Weighted Gene Co-Expression Network Analysis for Feather Follicle Density in a Chinese Indigenous Breed

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