Notch-induced transcription factors are predictive of survival and 5-fluorouracil response in colorectal cancer patients

Candy, Patrick A.; Phillips, Michael; Redfern, Andrew; Colley, Shane M.; Davidson, Jennifer; Stuart, Lisa M.; Wood, Brian; Zeps, Nikolajs; Leedman, Peter J.

doi:10.1038/bjc.2013.431

Cited by 56 publications

(58 citation statements)

References 50 publications

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“…The most investigated intestinal stem cell markers in a clinical setting are LGR5, 17,29-41 BMI1, 42-49 MSI1, 50-52 and SOX9. 5,28,[53][54][55][56][57][58][59][60][61] This review evaluates the potential clinical implications of these 4 putative intestinal stem cell markers and their potential role in human CRC.…”

Section: Introductionmentioning

confidence: 99%

Clinical Implications of Intestinal Stem Cell Markers in Colorectal Cancer

Espersen

Olsen

Linnemann

et al. 2015

Clinical Colorectal Cancer

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Colorectal cancer (CRC) still has one of the highest incidence and mortality rate among cancers. Therefore, improved differential diagnostics and personalized treatment are still needed. Several intestinal stem cell markers have been found to be associated with CRC and might have a prognostic and predictive significance in CRC patients. This review provides an overview of the intestinal stem cell markers leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5), B cell-specific Moloney murine leukemia virus insertion site 1 (BMI1), Musashi1 (MSI1), and sex-determining region y-box 9 (SOX9) and their implications in human CRC. The exact roles of the intestinal stem cell markers in CRC development and progression remain unclear; however, high expression of these stem cell markers have a potential prognostic significance and might be implicated in chemotherapy resistance.

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Section: Introductionmentioning

confidence: 99%

Clinical Implications of Intestinal Stem Cell Markers in Colorectal Cancer

Espersen

Olsen

Linnemann

et al. 2015

Clinical Colorectal Cancer

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“…Furthermore, detecting cells positive for CD133, OCT4, and SOX2 after chemoradiotherapy confirmed the role of undifferentiated cancer cells in tumor recurrence [232]. Additionally, it has been proposed that SOX9 is involved in colon carcinogenesis and cancer progression, due to its overexpression in CRC tissues and cell lines [233][234][235][236].…”

Section: Colon and Rectummentioning

confidence: 83%

Cancer stem cells in human digestive tract malignancies

2015

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Digestive tract malignancies, including oral, pharyngeal, esophageal, gastric, and colorectal cancers, are among the top 10 most common cancers worldwide. In spite of using various treatment modalities, cancer patients still suffer from recurrence and metastasis of malignant cells. Cancer stem cells (CSCs) are undifferentiated and highly proliferative malignant cells with unique properties mediated by overexpression of stemness markers, metastasis-related proteins, drug transporters, and DNA repair machinery. Due to their salient characteristics, it has been suggested that CSCs are responsible for tumor initiation, progression, invasion, recurrence, and therapy resistance. Exploring different aspects of CSC biology has fueled a great enthusiasm in designing novel therapeutic strategies to help patients. For instance, identification of markers associated with digestive tract CSCs, such as CD44, CD133, CD24, EpCAM, LGR5, ALDH1, and BMI1, has made it possible to develop more accurate diagnosis approaches. In addition, specifically targeting CSCs by their markers imposes fewer side effects and improves therapeutic outcomes. Here, we focus on the current status of CSC biology in digestive tract cancers, with emphasis on CSC markers, and review achieved progress in eradication of digestive tract CSC cells.

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“…Among them, FOXA1, STAT3 and HEY1 were more important in the regulatory network. Candy et al (37) indicated that overexpressed HEY1 was a negative prognostic factor for colorectal cancer, and it is closely associated with vascular and perineural invasion and lymph node metastasis. Therefore, the upregulated HEY1 may be associated with OS metastasis.…”

Section: Discussionmentioning

confidence: 99%

Common mechanism of pathogenesis in various types of metastatic osteosarcoma

2017

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Abstract. The present study aimed to investigate the common metastatic mechanism in various types of metastatic osteosarcoma (OS). Gene expression profiles generated from the metastatic OS KHOS and KRIB cell lines and the non-metastatic OS HOS cell line were compared. Two groups of differentially expressed genes (DEGs) between KHOS or KRIB and HOS were screened (P<0.01 and |fold change| ≥2) and then underwent Gene Ontology (GO) and pathway enrichment analyses. Subsequently, the protein-protein interaction (PPI) network was constructed and the subnetwork was mined. Furthermore, overlapping DEGs of these two groups were identified and pathway enrichment and regulatory network analyses were performed. A total of 1,552 and 1,330 DEGs from KHOS vs. HOS and KRIB vs. HOS were obtained, respectively. GO and pathway enrichment analyses of DEGs between KRIB and HOS, including anatomical structure morphogenesis and focal adhesion, were similar to those between KHOS and HOS. Vascular endothelial growth factor A and epidermal growth factor receptor were hub nodes in the PPI network for KHOS and KRIB. Subnetworks of these two groups were similar. In addition, 421 upregulated and 595 downregulated overlapping genes were enriched in the mitogen-activated protein kinase and transforming growth factor-β signaling pathways. Furthermore, seven vital transcription factors, including hes-related family bHLH transcription factor with YRPW motif 1 (HEY1), were obtained. Overall, different types of metastatic OS were shown to exhibit a similar mechanism of pathogenesis. With the exception of cell adhesion and angiogenesis, recapitulation of the morphogenetic processes facilitates OS tumor formation and metastasis. Genes such as HEY1 are important for metastatic OS. Further studies are required in order to confirm these results. IntroductionOsteosarcoma (OS), which is one of the common primary bone tumors in children and adolescents is highly aggressive and metastatic (1); it comprises ~5% of all pediatric tumors and patients with pulmonary metastasis present a poor prognosis (2). There are definite differences in the mechanism between primary and metastatic OS, and numerous previous studies have been performed to expound them (3-5).Multiple signaling pathways, including the Notch signaling pathway, are involved in cancer migration initiation through the extracellular matrix (ECM) towards the bloodstream (6). Survival of cancer cells in the bloodstream is mediated by the integrin signaling pathway to activate the phosphatidylinositol 3-kinase/protein kinase B survival pathway (7). Signaling pathways, including those of Src and Wnt, are involved in apoptosis resistance throughout metastasis (8,9). In addition, the immune system is also invaded and modulated for survival advantage (10). Subsequently, cell adhesion is arrested, and the cells extravasate to their new environment and re-establish cell-cell adhesions (11). There are numerous various viewpoints regarding the mechanism underlying metastatic tumor cell arrest to distant organ sit...

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Notch-induced transcription factors are predictive of survival and 5-fluorouracil response in colorectal cancer patients

Cited by 56 publications

References 50 publications

Clinical Implications of Intestinal Stem Cell Markers in Colorectal Cancer

Clinical Implications of Intestinal Stem Cell Markers in Colorectal Cancer

Cancer stem cells in human digestive tract malignancies

Common mechanism of pathogenesis in various types of metastatic osteosarcoma

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