Clinical Significance of Serum COL6A3 in Pancreatic Ductal Adenocarcinoma

Kang, Changshin; Wang, Jonathan; Axell-House, Dierdre B; Soni, Pranay; Chu, Mon‐Li; Chipitsyna, Galina; Sarosiek, Konrad; Sendecki, Jocelyn; Hyslop, Terry; Zoubi, Mazhar Salim Al; Yeo, Charles J.; Arafat, Hwyda A.

doi:10.1007/s11605-013-2326-y

Cited by 49 publications

(32 citation statements)

References 30 publications

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“…In addition, a growing body of evidence shows that ColVI is a potential biomarker for cancer diagnosis. ColVI levels in the sera of individuals with melanoma or pancreatic cancer are dramatically increased when compared with those of healthy controls (Burchardt et al, 2003;Makawita et al, 2011;Kang et al, 2014). Collectively, these findings point to ColVI as an ECM molecule that promotes tumor growth.…”

Section: Box 2 Collagen VI In Cancermentioning

confidence: 84%

Collagen VI at a glance

Cescon

Gattazzo

Chen

et al. 2015

Journal of Cell Science

285

286

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Collagen VI represents a remarkable extracellular matrix molecule, and in the past few years, studies of this molecule have revealed its involvement in a wide range of tissues and pathological conditions. In addition to its complex multi-step pathway of biosynthesis and assembly that leads to the formation of a characteristic and distinctive network of beaded microfilaments in the extracellular matrix, collagen VI exerts several key roles in different tissues. These range from unique biomechanical roles to cytoprotective functions in different cells, including myofibers, chondrocytes, neurons, fibroblasts and cardiomyocytes. Indeed, collagen VI has been shown to exert a surprisingly broad range of cytoprotective effects, which include counteracting apoptosis and oxidative damage, favoring tumor growth and progression, regulating autophagy and cell differentiation, and even contributing to the maintenance of stemness. In this Cell Science at a Glance article and the accompanying poster, we present the current knowledge of collagen VI, and in particular, discuss its relevance in stemness and in preserving the mechanical properties of tissues, as well as its links with human disorders.

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Section: Box 2 Collagen VI In Cancermentioning

confidence: 84%

Collagen VI at a glance

Cescon

Gattazzo

Chen

et al. 2015

Journal of Cell Science

285

286

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show abstract

“…Previous studies suggested that the induction of collagens including COL1A1 and COL4A1 is regulated by chemokine signaling (CXCR7) and downstream pathways such as PI3K/AKT and NF-κB [31, 32]. COL6A3, an ECM protein, has been identified as the clinically relevant collagen in colorectal, ovarian, and pancreatic cancer [36–38]. COL6A3 protein and mRNA are significantly upregulated not only in colorectal cancer cells but also in the stromal cells of tumor lesions, which promote tumor growth by modulating Hippo and Wnt signaling [36, 39].…”

Section: Discussionmentioning

confidence: 99%

Collagen type IV alpha 1 (COL4A1) and collagen type XIII alpha 1 (COL13A1) produced in cancer cells promote tumor budding at the invasion front in human urothelial carcinoma of the bladder

et al. 2017

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Current knowledge of the molecular mechanism driving tumor budding is limited. Here, we focused on elucidating the detailed mechanism underlying tumor budding in urothelial cancer of the bladder. Invasive urothelial cancer was pathologically classified into three groups as follows: nodular, trabecular, and infiltrative (tumor budding). Pathohistological analysis of the orthotopic tumor model revealed that human urothelial cancer cell lines MGH-U3, UM-UC-14, and UM-UC-3 displayed typical nodular, trabecular, and infiltrative patterns, respectively. Based on the results of comprehensive gene expression analysis using microarray (25 K Human Oligo chip), we identified two collagens, COL4A1 and COL13A1, which may contribute to the formation of the infiltrative pattern. Visualization of protein interaction networks revealed that proteins associated with connective tissue disorders, epithelial-mesenchymal transition, growth hormone, and estrogen were pivotal factors in tumor cells. To evaluate the invasion pattern of tumor cells in vitro, 3-D collective cell invasion assay using Matrigel was performed. Invadopodial formation was evaluated using Gelatin Invadopodia Assay. Knockdown of collagens with siRNA led to dramatic changes in invasion patterns and a decrease in invasion capability through decreased invadopodia. The in vivo orthotopic experimental model of bladder tumors showed that intravesical treatment with siRNA targeting COL4A1 and COL13A1 inhibited the formation of the infiltrative pattern. COL4A1 and COL13A1 production by cancer cells plays a pivotal role in tumor invasion through the induction of tumor budding. Blocking of these collagens may be an attractive therapeutic approach for treatment of human urothelial cancer of the bladder.

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“…1). 5,6,[8][9][10][11] This stroma creates a shield which prevents correct vascularization, hence reduces chemotherapies penetrance, and triggers the appearance of hypoxic zones, one of the most important characteristics of PDAC ( Fig. 1).…”

mentioning

confidence: 99%

Metabolic rewiring of pancreatic ductal adenocarcinoma: New routes to follow within the maze

Olivares

Vasseur

2015

Intl Journal of Cancer

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Pancreatic ductal adenocarcinoma (PDAC) is a debilitating and almost universally fatal malignancy. Despite advances in understanding of the oncogenetics of the disease, very few clinical benefits have been shown. One of the main characteristics of PDAC is the tumor architecture where tumor cells are surrounded by a firm desmoplasia. By reducing vascularization, thus both oxygen and nutrients delivery to the tumor, this stroma causes the appearance of hypoxic zones driving metabolic adaptation in surviving tumor cells in order to cope with challenging conditions. This metabolic reprogramming promoted by environmental constraints enhances PDAC aggressiveness. In this review, we provide a brief overview of previous works regarding the importance of glucose and glutamine addiction of PDAC cells. In particular we aim to highlight the need for exploring the impact of metabolites other than glucose and glutamine, such as non-essential amino acids and oncometabolites, to find new treatments. We also discuss the need for progress in methodology for metabolites detection. The overall purpose of our review is to emphasize the need to look beyond what is currently known, with a focus on amino acid availability, in order to improve our understanding of PDAC biology.Despite important scientific advances, pancreatic ductal adenocarcinoma (PDAC) remains a fatal cancer, offering one of the poorest prognosis and survival range.

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Clinical Significance of Serum COL6A3 in Pancreatic Ductal Adenocarcinoma

Cited by 49 publications

References 30 publications

Collagen VI at a glance

Collagen VI at a glance

Collagen type IV alpha 1 (COL4A1) and collagen type XIII alpha 1 (COL13A1) produced in cancer cells promote tumor budding at the invasion front in human urothelial carcinoma of the bladder

Metabolic rewiring of pancreatic ductal adenocarcinoma: New routes to follow within the maze

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