Knockdown of PSF1 expression inhibits cell proliferation in lung cancer cells in vitro

Zhang, Jingyao; Wu, Qifei; Wang, Zhe; Zhang, Yong; Zhang, Guangjian; Fu, Junke; Liu, Chang

doi:10.1007/s13277-014-2826-8

Cited by 31 publications

(29 citation statements)

References 19 publications

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“…GINS1 (also known as PSF1 ) is a subunit of the GINS (Go, lchi, Nii, San) complex which drives the unwinding of DNA in front of the replication fork [ 41 ]. Many studies have shown that GINS1 is up-regulated in several cancer types including lung, colon, prostate, colorectal and breast cancers [ 41 , 42 , 43 , 44 , 45 , 46 , 47 ]. It is reported that GINS1 is expressed widely in early embryogenesis in mice, stem and progenitor cells, etc.…”

Section: Discussionmentioning

confidence: 99%

Identification of Key Pathways and Genes in the Dynamic Progression of HCC Based on WGCNA

Cai

Zhu

et al. 2018

Genes

146

127

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Hepatocellular carcinoma (HCC) is a devastating disease worldwide. Though many efforts have been made to elucidate the process of HCC, its molecular mechanisms of development remain elusive due to its complexity. To explore the stepwise carcinogenic process from pre-neoplastic lesions to the end stage of HCC, we employed weighted gene co-expression network analysis (WGCNA) which has been proved to be an effective method in many diseases to detect co-expressed modules and hub genes using eight pathological stages including normal, cirrhosis without HCC, cirrhosis, low-grade dysplastic, high-grade dysplastic, very early and early, advanced HCC and very advanced HCC. Among the eight consecutive pathological stages, five representative modules are selected to perform canonical pathway enrichment and upstream regulator analysis by using ingenuity pathway analysis (IPA) software. We found that cell cycle related biological processes were activated at four neoplastic stages, and the degree of activation of the cell cycle corresponded to the deterioration degree of HCC. The orange and yellow modules enriched in energy metabolism, especially oxidative metabolism, and the expression value of the genes decreased only at four neoplastic stages. The brown module, enriched in protein ubiquitination and ephrin receptor signaling pathways, correlated mainly with the very early stage of HCC. The darkred module, enriched in hepatic fibrosis/hepatic stellate cell activation, correlated with the cirrhotic stage only. The high degree hub genes were identified based on the protein-protein interaction (PPI) network and were verified by Kaplan-Meier survival analysis. The novel five high degree hub genes signature that was identified in our study may shed light on future prognostic and therapeutic approaches. Our study brings a new perspective to the understanding of the key pathways and genes in the dynamic changes of HCC progression. These findings shed light on further investigations.

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Section: Discussionmentioning

confidence: 99%

Identification of Key Pathways and Genes in the Dynamic Progression of HCC Based on WGCNA

Cai

Zhu

et al. 2018

Genes

146

127

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“…Recently, several studies have shown that each GINS member is associated with malignant progression in several different tumor histotypes, i.e., PSF1 for breast cancer 3 , colon cancer 4 , and lung cancer 5 , PSF2 for cholangiocarcinoma 6 , and PSF3 for colon cancer 7 and non-small cell lung cancer 8 . Although we previously reported on the levels of expression of SLD5 in different cancer cell lines 7 , to the best of our knowledge there have been no reports thus far on its expression and malignant tumor progression.…”

mentioning

confidence: 99%

Regulation of SLD5 gene expression by miR-370 during acute growth of cancer cells

Yamane

Naito

Wakabayashi

et al. 2016

Sci Rep

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SLD5 is a member of the GINS complex, essential for DNA replication in eukaryotes. It has been reported that SLD5 is involved in early embryogenesis in the mouse, and cell cycle progression and genome integrity in Drosophila. SLD5 may be involved in malignant tumor progression, but its relevance in human cancer has not been determined. Here, we found strong SLD5 expression in both human bladder cancer tissues from patients and cell lines. Knockdown of SLD5 using small interfering RNA resulted in reduction of cell growth both in vitro and an in vivo xenograft model. Moreover, we found that high levels of SLD5 in bladder cancer cells result from downregulation of microRNA (miR)-370 that otherwise suppresses its expression. High level expression of DNA-methyltransferase (DNMT) 1 and IL-6 were also observed in bladder cancer cells. Knockdown of IL-6 led to downregulation of DNMT1 and SLD5 expression, suggesting that IL-6-induced overexpression of DNMT1 suppresses miR-370, resulting in high SLD5 expression. Our findings could contribute to understanding tumorigenic processes and progression of human bladder cancer, whereby inhibition of SLD5 could represent a novel strategy to prevent tumor growth.

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“…Overexpression of the GINS subunits were also reported in cancers. Psf1 was relatively highly expressed in breast tumor and lung cancer cells (Nakahara et al, 2010 ; Zhang J. et al, 2015 ). An increased ability of cancer cells to proliferate by Psf1 overexpression was observed by a mouse xenograft model (Nagahama et al, 2010b ).…”

Section: The Cmg As a Potential Target For Cancer Therapymentioning

confidence: 99%

The Human Replicative Helicase, the CMG Complex, as a Target for Anti-cancer Therapy

Seo

Kang

2018

Front. Mol. Biosci.

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DNA helicases unwind or rearrange duplex DNA during replication, recombination and repair. Helicases of many pathogenic organisms such as viruses, bacteria, and protozoa have been studied as potential therapeutic targets to treat infectious diseases, and human DNA helicases as potential targets for anti-cancer therapy. DNA replication machineries perform essential tasks duplicating genome in every cell cycle, and one of the important functions of these machineries are played by DNA helicases. Replicative helicases are usually multi-subunit protein complexes, and the minimal complex active as eukaryotic replicative helicase is composed of 11 subunits, requiring a functional assembly of two subcomplexes and one protein. The hetero-hexameric MCM2-7 helicase is activated by forming a complex with Cdc45 and the hetero-tetrameric GINS complex; the Cdc45-Mcm2-7-GINS (CMG) complex. The CMG complex can be a potential target for a treatment of cancer and the feasibility of this replicative helicase as a therapeutic target has been tested recently. Several different strategies have been implemented and are under active investigations to interfere with helicase activity of the CMG complex. This review focuses on the molecular function of the CMG helicase during DNA replication and its relevance to cancers based on data published in the literature. In addition, current efforts made to identify small molecules inhibiting the CMG helicase to develop anti-cancer therapeutic strategies were summarized, with new perspectives to advance the discovery of the CMG-targeting drugs.

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Knockdown of PSF1 expression inhibits cell proliferation in lung cancer cells in vitro

Cited by 31 publications

References 19 publications

Identification of Key Pathways and Genes in the Dynamic Progression of HCC Based on WGCNA

Identification of Key Pathways and Genes in the Dynamic Progression of HCC Based on WGCNA

Regulation of SLD5 gene expression by miR-370 during acute growth of cancer cells

The Human Replicative Helicase, the CMG Complex, as a Target for Anti-cancer Therapy

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