Overexpression ofCDCA5,KIF4A,TPX2, andFOXM1Coregulated Cell Cycle and Promoted Hepatocellular Carcinoma Development

“…CDCA5 is required for the stable binding of adhesion and chromatin in the G2/M phase and plays a vital role in cell cycle regulation. Researchers have found that CDCA5 can affect the cell division cycle in several tumours (23). Thus, the effects CDCA5 on the prostate cancer cell division cycle were explored.…”

Section: Cdca5 Regulates the Prostate Cancer Cell Division Cyclementioning

confidence: 99%

CDCA5 promotes the progression of prostate cancer by affecting the ERK signalling pathway

Shen

et al. 2021

Oncol Rep

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Cell division cycle-associated 5 (CDCA5) can regulate cell cycle-related proteins to promote the proliferation of cancer cells. The purpose of the present study was to investigate the expression level of CDCA5 in prostate cancer (PCa) and its effect on PCa progression. The signalling pathway by which CDCA5 functions through was also attempted to elucidate. Clinical specimens of PCa patients were collected from the Second Hospital of Tianjin Medical University. The expression level of CDCA5 in cancer tissues and paracancerous tissues from PCa patients was detected by RT-qPCR analysis and IHC. The relationship between the expression level of CDCA5 and the survival rate of PCa patients was analysed using TCGA database. Two stable cell lines (C4-2 and PC-3) with CDCA5 knockdown were established, and the effects of CDCA5 on PCa cell proliferation were detected by MTT and colony formation assays. Flow cytometry was performed to detect the effect of CDCA5 on the PCa cell division cycle, and western blot analysis was used to determine changes in ERK phosphorylation levels after CDCA5 knockdown. The effect of CDCA5 expression on prostate tumour growth was assessed using a mouse xenograft model. The results revealed that the mRNA and protein expression levels of CDCA5 were significantly higher in PCa tissues than in paracancerous tissues. High CDCA5 expression was associated with the prognosis of patients with PCa. CDCA5 expression knockdown significantly reduced the number of PCa cells in mitoses and inhibited their proliferation in vitro and in vivo . When CDCA5 was knocked down, the phosphorylation level of ERK was also reduced. Collectively, CDCA5 was upregulated and affected the prognosis of patients with PCa. Decreased CDCA5 expression inhibited PCa cell proliferation by inhibiting the ERK signalling pathway. Thus, CDCA5 may be a potential therapeutic target for PCa.

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“…Downward-regulated expression of CDCA5 [30,31], NDC80 [32], CCNA2 [33] on SNRPD1 silencing suggested reduced synthesis of DNA and proteins as well as recessed cell mitosis. Further evidence on reduced CCND1 expression after knocking down SNRPD1 implicated the accumulation of cells in the G 0 /G 1 state given the regulatory role of CCND1 in triggering G 0 /G 1 cell cycle arrest [29].…”

Section: Discussionmentioning

confidence: 98%

SNRPD1 confers diagnostic and therapeutic values on breast cancers through cell cycle regulation

Dai

Chen³

et al. 2021

Preprint

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Background: SNRPD1 is a spliceosome-associated protein and has previously been implicated with important roles in cancer development. Methods: Through analyzing the differential expression patterns and clinical association of splicing associated genes among tumor and tumor adjacent samples across different tumors and among different breast cancer subtypes, we identify the tumor promotive role of SNRPD1 using multiple publicly available datasets. Through pathway, gene ontology enrichment analysis and network construction, we linked the onco-therapeutic role of SNRPD1 with cell cycle. Via a series of experimental studies including knockdown assay, qPCR, western blotting, cell cycle, drug response assay, we confirmed the higher expression of SNPRD1 at both gene and protein expression levels in triple negative breast cancer cells, as well as its roles in promoting cell cycle and chemotherapy response.Results: Our study revealed that SNRPD1 over-expression was significantly associated with genes involved in cell cycle, cell mitosis and chromatin replication, and silencing SNRPD1 in breast cancer cells could lead to halted tumor cell growth and cell cycle arrest at the G0/G1 stage. We also found that triple negative breast cancer cells with reduced SNRPD1 expression lost certain sensitivity to doxorubicin whereas luminal cancer cells did not.Conclusions: Our results suggested the prognostic value of SNRPD1 on breast cancer survival, its potential as the therapeutic target halting cell cycle progression for breast cancer control, and warranted special attention on the combined use of doxorubicin and drugs targeting SNRPD1.

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Overexpression ofCDCA5,KIF4A,TPX2, andFOXM1Coregulated Cell Cycle and Promoted Hepatocellular Carcinoma Development

Cited by 20 publications

References 50 publications

Identification of Crucial Genes Associated With Immune Cell Infiltration in Hepatocellular Carcinoma by Weighted Gene Co-expression Network Analysis

Identification of Crucial Genes Associated With Immune Cell Infiltration in Hepatocellular Carcinoma by Weighted Gene Co-expression Network Analysis

CDCA5 promotes the progression of prostate cancer by affecting the ERK signalling pathway

SNRPD1 confers diagnostic and therapeutic values on breast cancers through cell cycle regulation

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