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Mutant collagen COL11A1 enhances cancerous invasion [RNA-seq]

ABSTRACT: RNA-seq was used to define the role of mutant COL11A1 in cutaneous squamous cell carcinoma (cSCC) by comparing human cSCC organoids edited to introduce the COL11A1 G598A substitution to organoids edited with an A to T substitution that preserves the native glycine residue while controlling for non-specific editing effects.

ORGANISM(S): Homo sapiens

PROVIDER: GSE178870 | GEO | 2021/07/23

REPOSITORIES: GEO

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Mutant collagen COL11A1 enhances cancerous invasion

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RNA-seq analysis of A2780 and OVCAR3 human ovarian cancer cell lines after overexpression of collagen type XI alpha 1 (COL11A1)

Project description:Collagen type XI alpha 1 (COL11A1) is identified as one of the most upregulated genes in cisplatin-resistant ovarian cancer and recurrent ovarian cancer. However, the exact functions of COL11A1 in cisplatin resistance are unknown. The goal of this study is to determine molecular mechanisms by which COL11A1 confers cisplatin resistance in ovarian cancer cells. We overexpressed COL11A1 in A2780 and OVCAR3 ovarian cancer cells, which express very low endogenous levels of COL11A1. We then compared the mRNA expression levels of various genes between COL11A1-overexpressing ovarian cancer cells and control ovarian cancer cells by RNA-Seq. Our RNA-Seq data show that COL11A1 overexpression did not consistently change the expression levels of genes involved in cisplatin efflux, glutathione metabolism, and DNA repair pathways, which are known to contribute to cisplatin resistance. This result implies that COL11A1 might confer cisplatin resistance in ovarian cancer cells through other mechanisms.

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COL11A1 promotes tumor progression and predicts poor clinical outcome in ovarian cancer.

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COL11A1 promotes tumor progression and predicts poor clinical outcome in ovarian cancer.

Project description:Biomarkers that predict disease progression might assist the development of better therapeutic strategies for aggressive cancers, such as ovarian cancer. Here, we investigated the role of collagen type XI alpha 1 (COL11A1) in cell invasiveness and tumor formation and the prognostic impact of COL11A1 expression in ovarian cancer. Microarray analysis suggested that COL11A1 is a disease progression-associated gene that is linked to ovarian cancer recurrence and poor survival. Whole tumor gene expression profiling was conducted on tissue samples from 60 ovarian cancer patients, and characteristics and clinico-pathological features of the patients are provided. We used several steps to analyze the expression profiles of the samples to identify the genes whose expression values correlate with survival, recurrence and advanced disease stage. First, using hazard ratios from univariate Cox regression analysis, the top 200 survival-related genes were evaluated for intersection with the top 200 recurrence-related genes, and 44 genes were obtained. Second, we examined the 44 genes that met the criteria of fold-change values between advanced stage and early stage samples of greater than 2 or less than 0.5. Ultimately, 17 genes were identified. A heat map of the 17 genes is depicted in the associated publication. Gene ontology and pathway enrichment analyses of the 17 genes were performed using Database for Annotation, Visualization and Integrated Discovery (DAVID). The major cellular component, biological process and molecular function of the 17 genes are associated with the extracellular region, intracellular signaling cascade, and protein binding and bridging, respectively. Two genes, COL11A1 and COL4A6, are involved in ECM-receptor interaction pathways. Notably, COL11A1 displayed the highest fold-change value in ovarian cancer disease progression; therefore, we selected COL11A1 for further experimental analysis.

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Inhibition of Collagen XI alpha 1–induced Fatty Acid Oxidation Triggers Apoptotic Cell Death in Cisplatin-Resistant Ovarian Cancer

Project description:Collagen type XI alpha 1 (COL11A1) is a novel biomarker associated with cisplatin resistance in ovarian cancer. However, the mechanisms underlying how COL11A1 confers cisplatin resistance in ovarian cancer are poorly understood. We identified that fatty acid β-oxidation (FAO) is upregulated by COL11A1 in ovarian cancer cells and that COL11A1-driven cisplatin resistance can be abrogated by inhibition of FAO. Furthermore, our results demonstrate that COL11A1 also enhances the expression of proteins involved in fatty acid synthesis. Interestingly, COL11A1-induced upregulation of fatty acid synthesis and FAO is modulated by the same signaling molecules. We identified that binding of COL11A1 to its receptors, α1β1 integrin and discoidin domain receptor 2 (DDR2), activates Src-Akt-AMPK signaling to increase the expression of both fatty acid synthesis and oxidation enzymes, although DDR2 seems to be the predominant receptor. Inhibition of fatty acid synthesis downregulates FAO despite the presence of COL11A1, suggesting that fatty acid synthesis might be a driver of FAO in ovarian cancer cells. Taken together, our results suggest that COL11A1 upregulates fatty acid metabolism in ovarian cancer cells in a DDR2-Src-Akt-AMPK dependent manner. Therefore, we propose that blocking FAO might serve as a promising therapeutic target to treat ovarian cancer, particularly cisplatin-resistant recurrent ovarian cancers which typically express high levels of COL11A1.

2020-04-28 | PXD016244 | Pride

COL11A1 mutations in cutaneous squamous cell carcinoma [WES]

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