Cell Cycle Regulation in Treatment of Breast Cancer

Cai, Zijie; Liu, Qiang

doi:10.1007/978-981-10-6020-5_12

Cited by 25 publications

(26 citation statements)

References 129 publications

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“…Consistent with the results of a previous study, the present results indicated that cell cycle progression and the AKT signaling pathway were significantly dysregulated in patients with breast cancer (28). The EGFR downstream AKT/Skp2associated pathway has a crucial role in regulating the cell cycle and cell proliferation in tumorigenesis (29).…”

Section: Discussionsupporting

confidence: 92%

USP18 promotes breast cancer growth by upregulating EGFR and activating the AKT/Skp2 pathway

et al. 2018

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Recent studies have suggested that ubiquitin-specific peptidase (USP)18 may act as an oncogene in various types of cancer. Although the role of USP18 in breast cancer cell lines has been elucidated, the underlying mechanisms and clinical role of USP18 in breast cancer are currently not well understood. The bioinformatics analysis and experimental results of the present study demonstrated that aberrant promoter methylation led to increased expression of USP18 in breast cancer. In addition, correlation analysis suggested that a negative correlation between methylation and USP18 mRNA expression was observed in The Cancer Genome Atlas database. USP18 promoted cell proliferation, colony formation and cell cycle progression in vitro. Furthermore, the Gene Set Enrichment Analysis results demonstrated that USP18 may be negatively associated with apoptosis in patients with breast cancer. Bioinformatics analysis results indicated that USP18 was also revealed to be associated with the protein kinase B (AKT) signaling pathway and mammary tumorigenesis in vivo. In addition, the results indicated that USP18 may promote the epidermal growth factor (EGF)-mediated EGF receptor (EGFR)/AKT/S‑phase kinase-associated protein 2 (Skp2) pathway by upregulating EGFR and Skp2 in a AKT/forkhead box O3-dependent manner in breast cancer. The results of bioinformatics analysis revealed that increased USP18 expression was associated with a higher TNM stage and unfavorable prognosis in clinical patients. USP18 was also significantly enhanced in patients with human epidermal growth factor receptor 2-positive breast cancer; furthermore, Kaplan‑Meier curve demonstrated that combining USP18 and Skp2 expression improved prognostic capability in breast cancer. Taken together, these results suggested that USP18 may serve a key role in breast cancer development by upregulating EGFR and subsequently activating the AKT/Skp2 feedback loop pathway. The role of USP18 in breast cancer provides a novel insight into the clinical application of the USP18/AKT/Skp2 pathway.

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Section: Discussionsupporting

confidence: 92%

USP18 promotes breast cancer growth by upregulating EGFR and activating the AKT/Skp2 pathway

et al. 2018

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“…Cell cycle control is a highly regulated process that involves a complex cascade of events. Modulation of the expression and function of cell cycle regulatory proteins provides an important approach for the inhibition of tumor growth (Cai and Liu, 2017). Our results showed that Cyclins (cyclin A2, B1, B2), CDK2, CDC2 were down-regulated in BTPs treated HepG2 cells, while CDK inhibitor p21WAF1 and other growth inhibitors BTG2 and VDUP1 were upregulated, suggesting that BTPs inhibit the growth of HepG 2 cells through the arrest of cell cycle and the inhibition of cell proliferation.…”

Section: Conflict Of Interestmentioning

confidence: 67%

Gene expression profiling of HepG2 cells after treatment with black tea polyphenols

Zhong

Deng²,

Jiang³

et al. 2018

Biocell

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This study aimed to determine the effects of black tea polyphenols on gene expression in hepatocellular cancer cells. The total Rna from hepg2 hepatocellular cancer cells treated with black tea polyphenols was subjected to human 14K cDna microarray analysis. Real-time PCR and Western blot analysis were conducted to verify microarray data. Black tea polyphenols treatment at the dose of 20 mg/L, 40 mg/L or 80 mg/L for one to three days inhibited the growth of hepg2 cells in a dose and time dependent manner. a total of 48 genes showed more than twofold change after black tea polyphenols treatment, including 17 upregulated genes and 31 downregulated genes, and they were involved in the regulation of cell growth, cell cycle, apoptosis, signaling, angiogenesis, tumor invasion and metastasis. Real-time PCR analysis of the selected genes showed that their mRna expression changes were consistent with the microarray data. in addition, Western blot analysis of the selected genes showed that their protein expression changes were consistent with mRna expression. in conclusion, gene expression profiles provide comprehensive molecular mechanisms by which black tea polyphenols exerts growth inhibition effects on cancer cells. The novel molecular targets identified in this study may be further exploited as therapeutic strategies for hepatocellular cancer.

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“…Considering the role of TGF-beta signaling pathways in tumors, it is inferred that SYNJ2 and its co-expressed genes can promote LUAD cells' in ltration and migration by TGF-beta signaling pathways. Since cancer is characterized by the deregulation of cell cycle activity that lead to aberrant cell proliferation [32][33], many authors have concluded that cancer can be regarded as a disease of the cell cycle [34]. Previous studies reported that many genes can regulate cell cycles to promote LC cell proliferations [35][36][37][38].…”

Section: Discussionmentioning

confidence: 99%

The Clinical Significance and Potential Molecular Mechanisms of Synaptojanin 2 in Lung Adenocarcinoma

Chen

et al. 2020

Preprint

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Background Lung adenocarcinoma (LUAD) is the main pathological type of pulmonary malignant tumors. Synaptojanin 2 (SYNJ2), a member of the synaptojanin family, is considered as an attractive underlying therapeutic target in several types of cancer. The purpose of the current research was to comprehensively investigate the molecular function and underlying mechanism of SYNJ2 in LUAD with the goal of providing a promising therapeutic target for LUAD. Methods We applied tissue microarrays, immunohistochemistry (IHC), high-throughput RNA sequencing (RNA-seq) data, and gene microarrays of public databases to comprehensively examine the protein level, mRNA expression, clinical significance, and prognosis value of SYNJ2 in LUAD. The standard mean difference (SMD) and summary receiver operating characteristic curves (SROC) were computed to evaluate the comprehensive expression value of SYNJ2 in LUAD. Kaplan-Meier survival curves were plotted to determine the overall survival of SYNJ2 with different expression levels in LUAD. Univariate and multivariate cox regression analyses were implemented to investigate the dependent prognostic ability of SYNJ2 expression and the clinically-relevant traits of LUAD. Moreover, SYNJ2 co-expressed genes were screened for Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) function analysis and protein–protein interactions (PPI) network construction. Results SYNJ2 overexpression in LUAD was confirmed by 2,299 LUAD samples and 1,387 non-tumor tissues obtained from tissue microarrays along with TCGA and public gene microarrays. The pooled SMD was 1.29 (95% CI: 1.09-1.48, I-square=78.6%, P<0.001) and the area under the curve (AUC) of the SROC was 0.88 (95%CI: 0.85-0.91). Compared to the upregulation of SYNJ2, SYNJ2 downregulation could improve OS in LUAD patients to some extent. SYNJ2 may facilitate the proliferation and progression of LUAD by modulating the cell cycle and TGF-beta signaling pathways. The 10 SYNJ2 co-expressed key genes selected from PPI network were all prominently implicated with the prognosis of LUAD patients. Conclusion SYNJ2 may contribute as an attractive and prospective therapeutic target in LUAD.

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Cell Cycle Regulation in Treatment of Breast Cancer

Cited by 25 publications

References 129 publications

USP18 promotes breast cancer growth by upregulating EGFR and activating the AKT/Skp2 pathway

USP18 promotes breast cancer growth by upregulating EGFR and activating the AKT/Skp2 pathway

Gene expression profiling of HepG2 cells after treatment with black tea polyphenols

The Clinical Significance and Potential Molecular Mechanisms of Synaptojanin 2 in Lung Adenocarcinoma

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