&lt;p&gt;Overexpression of shugoshin1 predicts a poor prognosis for prostate cancer and promotes metastasis by affecting epithelial&amp;ndash;mesenchymal transition&lt;/p&gt;

Mu, Jiagui; Fan, Li; Liu, Duo; Zhu, Dongsheng

doi:10.2147/ott.s191157

Cited by 16 publications

(17 citation statements)

References 21 publications

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“…For instance, SGOL1, a member of the shugoshin family of proteins, is thought to protect centromeric cohesion during mitosis, and its dysregulation at centromeres can lead to chromosome missegregation and miotic arrest [40, 41]. Mu et al found that SGOL1 expression levels are higher in prostate cancer tissues, and SGLO1 knockdown results in the inhibition of tumor cell proliferation, migration, and invasion [42]. In addition, SGOL1 has been found in other cancers (e.g., breast cancer and glioblastoma) [43–45].…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of DNA methylation and gene expression profiles in cholangiocarcinoma

Zhang

Meng

et al. 2019

Cancer Cell Int

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Background: The incidence of cholangiocarcinoma (CCA) has risen in recent years, and it has become a significant health burden worldwide. However, the mechanisms underlying tumorigenesis and progression of this disease remain largely unknown. An increasing number of studies have demonstrated crucial biological functions of epigenetic modifications, especially DNA methylation, in CCA. The present study aimed to identify and analyze methylationregulated differentially expressed genes (MeDEGs) involved in CCA tumorigenesis and progression by bioinformatics analysis. Methods:The gene expression profiling dataset (GSE119336) and gene methylation profiling dataset (GSE38860) were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and differentially methylated genes (DMGs) were identified using the limma packages of R and GEO2R, respectively. The MeDEGs were obtained by overlapping the DEGs and DMGs. Functional enrichment analyses of these genes were then carried out. Protein-protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape to determine hub genes. Finally, the results were verified based on The Cancer Genome Atlas (TCGA) database. Results:We identified 98 hypermethylated, downregulated genes and 93 hypomethylated, upregulated genes after overlapping the DEGs and DMGs. These genes were mainly enriched in the biological processes of the cell cycle, nuclear division, xenobiotic metabolism, drug catabolism, and negative regulation of proteolysis. The top nine hub genes of the PPI network were F2, AHSG, RRM2, AURKB, CCNA2, TOP2A, BIRC5, PLK1, and ASPM. Moreover, the expression and methylation status of the hub genes were significantly altered in TCGA. Conclusions:Our study identified novel methylation-regulated differentially expressed genes (MeDEGs) and explored their related pathways and functions in CCA, which may provide novel insights into a further understanding of methylation-mediated regulatory mechanisms in CCA.

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Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of DNA methylation and gene expression profiles in cholangiocarcinoma

Zhang

Meng

et al. 2019

Cancer Cell Int

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“…For instance, forkhead transcription factor (FoxM1) functions as an oncogene in the initiation, development, and progression of cancer, and its neoplastic functions can be used as a strong biomarker for the diagnosis and treatment of cancer (21). In prostate cancer, numerous prognostic biomarkers were also investigated (22)(23)(24). For instance, minichromosome maintenance 10 replication initiation factor (MCM10) was revealed to be significantly upregulated in prostate cancer patients, and overexpression of MCM10 promoted cell proliferation and predicted poor prognosis in prostate cancer (25).…”

Section: Discussionmentioning

confidence: 99%

Increased expression of CD81 is associated with poor prognosis of prostate cancer and increases the progression of prostate cancer cells in�vitro

Qian

Yang

2019

Exp Ther Med

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CD81, a member of the tetraspanin family, has been revealed to be upregulated and associated with prognosis in several types of cancer; however, this relationship has not been explored in prostate cancer. The present study aimed to investigate the prognostic significance and functional role of CD81 in prostate cancer. The expression of CD81 in prostate cancer tissues and cell lines was evaluated using qRT-PCR analysis. Kaplan-Meier survival analysis and Cox regression analysis were conducted to explore the prognostic significance of CD81. Cell experiments were used to explore the effects of CD81 on cell proliferation, migration, and invasion in prostate cell lines in vitro. The expression of CD81 was increased in both prostate cancer tissues and cell lines. Upregulation of CD81 was significantly associated with lymph node metastasis and TNM stage. Moreover, patients with high CD81 levels had poorer overall survival than those with lower levels. Additionally, tumor cell proliferation, migration, and invasion were inhibited by knockdown of CD81. The present results indicated that CD81 plays an oncogenic role in prostate cancer. Overexpression of CD81 may serve as a prognostic biomarker and therapeutic target and is involved in the progression of prostate cancer.

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“…29,31–33 Other authors have also shown a role for Sgo1 in tumorigenesis and EMT. 15,34 However, no study has linked Sgo1 to EMT in TNBC.…”

Section: Introductionmentioning

confidence: 99%

Mitotic kinases as drivers of the epithelial-to-mesenchymal transition and as therapeutic targets against breast cancers

Colón-Marrero

Jusino

Rivera-Rivera

et al. 2021

Exp Biol Med (Maywood)

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Biological therapies against breast cancer patients with tumors positive for the estrogen and progesterone hormone receptors and Her2 amplification have greatly improved their survival. However, to date, there are no effective biological therapies against breast cancers that lack these three receptors or triple-negative breast cancers (TNBC). TNBC correlates with poor survival, in part because they relapse following chemo- and radio-therapies. TNBC is intrinsically aggressive since they have high mitotic indexes and tend to metastasize to the central nervous system. TNBCs are more likely to display centrosome amplification, an abnormal phenotype that results in defective mitotic spindles and abnormal cytokinesis, which culminate in aneuploidy and chromosome instability (known causes of tumor initiation and chemo-resistance). Besides their known role in cell cycle control, mitotic kinases have been also studied in different types of cancer including breast, especially in the context of epithelial-to-mesenchymal transition (EMT). EMT is a cellular process characterized by the loss of cell polarity, reorganization of the cytoskeleton, and signaling reprogramming (upregulation of mesenchymal genes and downregulation of epithelial genes). Previously, we and others have shown the effects of mitotic kinases like Nek2 and Mps1 (TTK) on EMT. In this review, we focus on Aurora A, Aurora B, Bub1, and highly expressed in cancer (Hec1) as novel targets for therapeutic interventions in breast cancer and their effects on EMT. We highlight the established relationships and interactions of these and other mitotic kinases, clinical trial studies involving mitotic kinases, and the importance that represents to develop drugs against these proteins as potential targets in the primary care therapy for TNBC.

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<p>Overexpression of shugoshin1 predicts a poor prognosis for prostate cancer and promotes metastasis by affecting epithelial–mesenchymal transition</p>

Cited by 16 publications

References 21 publications

Comprehensive analysis of DNA methylation and gene expression profiles in cholangiocarcinoma

Comprehensive analysis of DNA methylation and gene expression profiles in cholangiocarcinoma

Increased expression of CD81 is associated with poor prognosis of prostate cancer and increases the progression of prostate cancer cells in�vitro

Mitotic kinases as drivers of the epithelial-to-mesenchymal transition and as therapeutic targets against breast cancers

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