DNA Replication and Sister Chromatid Cohesion 1 (DSCC1) of the Replication Factor Complex CTF18-RFC is Critical for Colon Cancer Cell Growth

Kim, Jong-Tae; Cho, Hee Jun; Park, Soo‐Jin; Oh, Byung Moo; Hwang, Yo Sep; Baek, Kyoung Eun; Lee, Young-Ha; Kim, Hee Cheol; Lee, Hee Gu

doi:10.7150/jca.32339

Cited by 9 publications

(8 citation statements)

References 40 publications

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“…When the cytoplasmic DSCC1 expression is higher in the tumor area, the survival probability of colon cancer patients is lower. [ 27 , 28 ] Some studies have explored DSCC1 as a potential tumor biomarker for early diagnosis and prognosis. By interfering with the function of DSCC1, proliferation and survival of tumor cells may be affected.…”

Section: Discussionmentioning

confidence: 99%

Roles of DSCC1 and GINS1 in gastric cancer

Hou,

Zhang,

Chi

et al. 2023

Medicine

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Gastric carcinoma is a common malignant tumor originating from gastric mucosal epithelium. However, role of DS-cell cycle-dependent protein 1 (DSCC1) and GINS1 in gastric carcinoma remains unclear. The gastric carcinoma datasets GSE79973 and GSE118916 were downloaded from gene expression omnibus. Multiple datasets were merged and batched. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. Functional enrichment analysis, gene set enrichment analysis and immune infiltration analysis were performed. Construction and analysis of protein-protein interaction Network. Survival analysis and comparative toxicogenomics database were performed. A heat map of gene expression was drawn. Target Scan screen miRNAs regulating DEGs. Two thousand forty-four DEGs were identified. According to gene ontology analysis, in biological process, they were mainly enriched in cell migration, transforming growth factor β receptor signaling pathway, angiogenesis, and steroid metabolism process. In cellular component, they were mainly enriched in extracellular vesicles, basement membrane, endoplasmic reticulum lumen, and extracellular space. In molecular function, they focused on extracellular matrix structural components, protein binding, platelet-derived growth factor binding, and catalytic activity. In Kyoto encyclopedia of genes and genomes, they were mainly enriched in protein digestion and absorption, metabolic pathways, fatty acid degradation, Glycerophospholipid metabolism, ether lipid metabolism. Gene set enrichment analysis showed that DEGs were mainly enriched in transforming growth factor β receptor signaling pathway, steroid metabolism process, basement membrane, endoplasmic reticulum lumen, structural components of extracellular matrix, platelet-derived growth factor binding, Glycerophospholipid metabolism, ether lipid metabolism. The results of immune infiltration analysis showed that expression of T cell CD4 memory resting was lower in the samples of gastric cancer. The core genes (TRIP13, CHEK1, DSCC1, GINS1) are protective factors, their expression shows a downward trend with increase of risk score. Comparative toxicogenomics database analysis showed that TRIP13, CHEK1, DSCC1, GINS1 were related to gastric tumors, gastric diseases, tumors, inflammation, and necrosis. DSCC1 and GINS1 are highly expressed in gastric cancer. Higher expression levels of DSCC1 and GINS1, worse the prognosis.

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Section: Discussionmentioning

confidence: 99%

Roles of DSCC1 and GINS1 in gastric cancer

Hou,

Zhang,

Chi

et al. 2023

Medicine

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“…Recently, overexpression of DSCC1 (DNA replication and sister chromatid cohesion 1) was found to increase proliferation, invasion and migration of breast carcinoma cells, as well as its knockdown showed opposite outcomes [ 43 , 44 ]. Besides, the authors found that DSCC1 could promote breast carcinoma progression by activating the Wnt/β-catenin signalling and inhibiting p53 protein.…”

Section: Discussionmentioning

confidence: 99%

In silico recognition of a prognostic signature in basal-like breast cancer patients

Conte

Sibilio

Grimaldi³

et al. 2022

PLoS ONE

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Background Triple-negative breast cancers (TNBCs) display poor prognosis, have a high risk of tumour recurrence, and exhibit high resistance to drug treatments. Based on their gene expression profiles, the majority of TNBCs are classified as basal-like breast cancers. Currently, there are not available widely-accepted prognostic markers to predict outcomes in basal-like subtype, so the selection of new prognostic indicators for this BC phenotype represents an unmet clinical challenge. Results Here, we attempted to address this challenging issue by exploiting a bioinformatics pipeline able to integrate transcriptomic, genomic, epigenomic, and clinical data freely accessible from public repositories. This pipeline starts from the application of the well-established network-based SWIM methodology on the transcriptomic data to unveil important (switch) genes in relation with a complex disease of interest. Then, survival and linear regression analyses are performed to associate the gene expression profiles of the switch genes with both the patients’ clinical outcome and the disease aggressiveness. This allows us to identify a prognostic gene signature that in turn is fed to the last step of the pipeline consisting of an analysis at DNA level, to investigate whether variations in the expression of identified prognostic switch genes could be related to genetic (copy number variations) or epigenetic (DNA methylation differences) alterations in their gene loci, or to the activities of transcription factors binding to their promoter regions. Finally, changes in the protein expression levels corresponding to the so far identified prognostic switch genes are evaluated by immunohistochemical staining results taking advantage of the Human Protein Atlas. Conclusion The application of the proposed pipeline on the dataset of The Cancer Genome Atlas (TCGA)-Breast Invasive Carcinoma (BRCA) patients affected by basal-like subtype led to an in silico recognition of a basal-like specific gene signature composed of 11 potential prognostic biomarkers to be further investigated.

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“…The role of RFC in human cancers, including CRC, has been identified. 7,9,10,[19][20][21] Although multiple pathological factors are involved in the progression of CRC, RFC regulates a range of tumor phenotypes, including proliferation, metastasis, and invasion. 7,21 Members of the RFC family are structurally and functionally similar.…”

Section: Rfc5 Knockdown Inhibits Crc Progression and May Affect The V...mentioning

confidence: 99%

RFC5, regulated by circ_0038985/miR‐3614‐5p, functions as an oncogene in the progression of colorectal cancer

Yao

Zhou

et al. 2023

Molecular Carcinogenesis

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Replication factor C 5 (RFC5) is involved in a variety of biological functions of cancer.However, the expression pattern of RFC5 and the underlying mechanisms in colorectal cancer (CRC) remain elusive. Here, we show that RFC5 is significantly upregulated in CRC tissues and cells. Patients with CRC and increased RFC5 levels have an unfavorable prognosis. RFC5 can promote the proliferation, migration, and invasion of CRC cells and inhibit the apoptosis of CRC cells. Additionally, upstream of RFC5, we constructed the competing endogenous RNA network and confirmed that RFC5 in this network was inhibited by miR-3614-5p by directly targeting its 3′-untranslated regions. We verified that circ_0038985, which is positively correlated with RFC5, directly targeted miR-3614-5p. Overexpression of circ_0038985 promoted CRC cell migration and invasion, and these effects were partially reversed by the reintroduction of miR-3614-5p. Moreover, we found that RFC5 may promote the vascular endothelial growth factor A (VEGFa)/vascular endothelial growth factor receptor 2 (VEGFR2)/extracellular signal-regulated protein kinase (ERK) pathway. The knockdown of RFC5 reduced CRC tumorigenesis in vivo.Collectively, these data demonstrate that the circ_0038985/miR-3614-5p/RFC5 axis plays a critical role in the progression of CRC, and RFC5 may promote CRC progression by affecting the VEGFa/VEGFR2/ERK pathway.

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DNA Replication and Sister Chromatid Cohesion 1 (DSCC1) of the Replication Factor Complex CTF18-RFC is Critical for Colon Cancer Cell Growth

Cited by 9 publications

References 40 publications

Roles of DSCC1 and GINS1 in gastric cancer

Roles of DSCC1 and GINS1 in gastric cancer

In silico recognition of a prognostic signature in basal-like breast cancer patients

RFC5, regulated by circ_0038985/miR‐3614‐5p, functions as an oncogene in the progression of colorectal cancer

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