CSN1 facilitates proliferation and migration of hepatocellular carcinoma cells by upregulating cyclin A2 expression

Fu, Hangwei; Zhang, Yida; Yin, Chang; Chen, Junying; Chen, Ping

doi:10.3892/mmr.2020.11684

Cited by 9 publications

(9 citation statements)

References 43 publications

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“…34 A report showed that CSN1 could enhance the proliferative and migrated abilities of MHCC-LM3 cells by upregulating CCNA2 expression. 35 Moreover, CCNA2 is active in the cytoplasm to activate PLK1 during the S/G2 transition. 36…”

Section: Discussionmentioning

confidence: 99%

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

Rong

Zhong

et al. 2021

Exp Biol Med (Maywood)

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In our studies, cyclin B1 ( CCNB1) mRNA and protein were overexpressed in hepatocellular carcinoma (HCC) tissues compared with non-HCC tissues. Moreover, CCNB1 was overexpressed in the serum of HCC patients. The expression of CCNB1 was associated with several crucial clinicopathologic characteristics, and the HCC patients with overexpressed CCNB1 had worse overall survival outcomes. In the screening of interactional genes, a total of 266 upregulated co-expression genes, which were positively associated with CCNB1, were selected from the datasets, and 67 downregulated co-expression genes, which were negatively associated with CCNB1, were identified. The key genes might be functionally enriched in DNA replication and the cell cycle pathways. CDC20, CCNA2, PLK1, and FTCD were selected for further research because they were highly connected in the protein-protein interaction networks. Upregulated CDC20, CCNA2, and PLK1 and downregulated FTCD might result in undesirable overall survival outcomes for HCC patients. The univariate Cox analysis results showed that CDC20 and PLK1 might be two independent risk factors, while FTCD might be protective in HCC. Therefore, CCNB1 may participate in the cell cycle of HCC by regulating DNA replication, and CCNB1 may provide a direction for the diagnosis of early-stage HCC and targeted HCC therapy.

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Section: Discussionmentioning

confidence: 99%

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

Rong

Zhong

et al. 2021

Exp Biol Med (Maywood)

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“…However, ubiquitination of substrates by APC/C requires activation or co-activation of CDC20 or CDH1 [ 46 , 47 , 48 ]. In addition to CCNA2 regulating cell proliferation by binding with CDC20 [ 49 ], CCNA2 is also regulated by CSN1 (signalosome subunit 1) in an ubiquitination-independent manner, which affects the proliferation and migration of hepatocellular carcinoma cells [ 50 ]. Surprisingly, the PPI network ( Figure 5 ) showed that the proteins controlling cell cycle progression (mRNAs were down-regulated, according to sequencing results) can interact with ubiquitin-proteasome-related proteins (mRNAs were up-regulated), which implies that ubiquitination of cell cycle-related proteins (such as CCNA2 and CDC20) determines cell development, and ubiquitination plays an indispensable role in the regulation of yak preadipocyte proliferation and differentiation by lncFAM200B .…”

Section: Discussionmentioning

confidence: 99%

Molecular Regulation of Yak Preadipocyte Differentiation and Proliferation by LncFAM200B and ceRNA Regulatory Network Analysis

Ran

Yang

Luo

et al. 2022

Cells

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The positive regulatory role of lncFAM200B in differentiation and lipid deposition in yak intramuscular preadipocytes has been demonstrated in our previous study. However, the regulatory mechanisms remain unclear. In this study, we aimed to produce complete mRNA and microRNA (miRNA) profiles after adenovirus-mediated lncFAM200B overexpression in yak preadipocytes using high-throughput sequencing. We constructed a competing endogenous RNA (ceRNA) network with lncFAM200B as the core and identified the functions of the selected target miRNA during cell proliferation and differentiation. We obtained 118 differentially expressed genes (DEGs) after lncFAM200B overexpression, 76 of which were up-regulated, including Notch signaling members NOTCH3, DTX3L, and HES4, and 42 DEGs were down-regulated, including genes related to the cell cycle (CCNA2, BUB1, CDC20, TOP2A, and KIF20A). Additionally, many ubiquitin-mediated proteolysis pathway members were also significantly up-regulated (BUA7, PML, TRIM21, and TRIM25). MiRNA sequencing showed that 13 miRNAs were significantly up-regulated, and 12 miRNAs were down-regulated. Among them, 29 targets of 10 differentially expressed miRNAs (DEMs) were differentially expressed, including miR-152-FBXO33, miR-6529a-TRIM21, miR-148c-NOTCH3, and the miR-6529b-HES4 axis. We further verified that overexpression and inhibition of miR-6529a can inhibit and promote, respectively, the proliferation and differentiation of preadipocytes. Taken together, our study not only revealed the regulatory network of lncFAM200B during yak preadipocytes differentiation but also laid a foundation for elucidating the cause for lower intramuscular fat content in yaks at the molecular level.

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“…Additionally, MGB1 and cyclins contributed to the regulation of the migration and invasion abilities of resistant cells. A previous study reported that the upregulation of cyclin A2 enhanced the migration of hepatocellular carcinoma (HCC), while its downregulation decreased the migration of DLD‐1 and SW620 colorectal cancer cell lines (CRC) [ 38 , 43 ]. Cyclin D1 enhances cell migration and invasion activity in fibroblasts by regulating RhoA [ 33 ] as well as tumor cells [ 34 , 35 , 44 ].…”

Section: Discussionmentioning

confidence: 99%

Mammaglobin 1 mediates progression of trastuzumab‐resistant breast cancer cells through regulation of cyclins and NF‐κB

et al. 2022

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Overexpression of human epidermal growth factor receptor 2 (HER2) in various cancers is correlated with poor patient survival. Trastuzumab, a recombinant humanized monoclonal antibody against HER2, has been considered to be a first-line therapy for HER2-positive breast cancer patients, but its usefulness is limited by the development of resistance. In this study, we established resistant cells by long-term treatment with trastuzumab. These cells showed higher proliferation, invasion, and migration abilities than the wild-type cells. Mammaglobin 1 (MGB1), cyclin D1, E1, A2, and phosphorylated NF-jB (p-p65) were upregulated in resistant cells. These proteins regulate cell proliferation, migration, and invasion of resistant cells. Depletion of MGB1 decreased cyclin and p-p65 expression. Cyclin D1 and A2, but not E1 expression, were affected by p-p65 downregulation. In summary, our results indicate that MGB1 expression is increased in breast cancer cells that have gained resistance to trastuzumab, and suggest that MGB1 promotes aggressiveness through cyclin and NF-jB regulation.Human epidermal growth factor receptor 2 (HER2), which belongs to the epidermal growth factor receptor (EGFR) superfamily, is a protein involved in one of the most studied signal transduction pathways in cancer [1]. The amplification or overexpression of HER2 is detected in 15-20% of breast [1], 17.9% of gastric and gastroesophageal cancer [2], in 20-30% of some ovarian cancer [3], and is correlated with poor patient survival. The estrogen receptor (ER) and HER2 (c-erbB2, HER2/neu) signaling pathways are the dominant drivers of cell proliferation and survival in the majority (85%) of breast cancer cases [4]. Under normal physiological conditions, HER2 activation is spatially and temporally controlled when the ligand binds to one of the other EGFR family members, leading to heterodimer formation with HER2, which then activates its kinase activity. However, in the abnormal condition, when HER2 is overexpressed, this molecule associates with itself and other EGFR family

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CSN1 facilitates proliferation and migration of hepatocellular carcinoma cells by upregulating cyclin A2 expression

Cited by 9 publications

References 43 publications

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

CCNB1 promotes the development of hepatocellular carcinoma by mediating DNA replication in the cell cycle

Molecular Regulation of Yak Preadipocyte Differentiation and Proliferation by LncFAM200B and ceRNA Regulatory Network Analysis

Mammaglobin 1 mediates progression of trastuzumab‐resistant breast cancer cells through regulation of cyclins and NF‐κB

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