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Mutant collagen COL11A1 enhances cancerous invasion [RNA-seq]

ABSTRACT: Mutant collagen COL11A1 enhances cancerous invasion [RNA-seq]

PROVIDER: PRJNA741266 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14908000_1.fastq.gz	Fastqsanger.gz
	SRR14908000_2.fastq.gz	Fastqsanger.gz
	SRR14908001_1.fastq.gz	Fastqsanger.gz
	SRR14908001_2.fastq.gz	Fastqsanger.gz
	SRR14908002_1.fastq.gz	Fastqsanger.gz

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Mutant collagen COL11A1 enhances cancerous invasion

Project description:Mutant collagen COL11A1 enhances cancerous invasion

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Mutant collagen COL11A1 enhances cancerous invasion [RNA-seq]

Project description: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.

2021-07-23 | GSE178870 | GEO

Mutant collagen COL11A1 enhances cancerous invasion.

Project description:Collagens are the most abundant proteins in the body and comprise the basement membranes and stroma through which cancerous invasion occurs; however, a pro-neoplastic function for mutant collagens is undefined. Here we identify COL11A1 mutations in 66 of 100 cutaneous squamous cell carcinomas (cSCCs), the second most common U.S. cancer, concentrated in a triple helical region known to produce trans-dominant collagens. Analysis of COL11A1 and other collagen genes found that they are mutated across common epithelial malignancies. Knockout of mutant COL11A1 impairs cSCC tumorigenesis in vivo. Compared to otherwise genetically identical COL11A1 wild-type tissue, gene-edited mutant COL11A1 skin is characterized by induction of β1 integrin targets and accelerated neoplastic invasion. In mosaic tissue, mutant COL11A1 cells enhanced invasion by neighboring wild-type cells. These results suggest that specific collagens are commonly mutated in cancer and that mutant collagens may accelerate this process.

| S-EPMC8566234 | biostudies-literature

Mutant collagen COL11A1 enhances cancerous invasion

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-23 | GSE179297 | GEO

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

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.

2019-10-10 | GSE112985 | GEO

Hypoxia induced ATF3 escalates breast cancer invasion by increasing collagen deposition

Project description:Activating transcription factors (ATFs), members of the adaptive-response gene family, participate in cellular processes to aid adaptations in response to extra- and/or intracellular changes. In this study, we observed that one of the ATFs Activating transcription factor 3 (ATF3) is upregulated under hypoxia via alterations in the epigenetic landscape of its promoter, followed by transcriptional upregulation. Under hypoxic conditions, Hypoxia-inducible factor 1-alpha (HIF1ɑ) alleviates methylation at the ATF3 promoter by recruiting TET1 and induces ATF3 transcription. Additionally, our RNA-seq analysis showed that ATF3 globally affects transcription under hypoxia and controls the processes of EMT and cancer invasion by stimulating the transcription of Prolyl 4-Hydroxylase Subunit Alpha 1 (P4HA1), an enzyme which enhances invasion conducive extracellular matrix (ECM) under hypoxic condition. Prolyl hydroxylases play a critical role in the hydroxylation and deposition of collagen in the extracellular matrix (ECM) during the evolution of cancer, which is necessary for metastasis. Importantly, P4HA1 undergoes alternative splicing under hypoxia, where the inclusion of exon 9a is increased. It is interesting to note that ATF3's involvement in P4HA1 splicing was also evident, as binding of ATF3 at intron 9a led to demethylation of this DNA region via recruitment of TET1. Further, we also show that the demethylated DNA region of intron 9a then becomes accessible to CTCF. Thus, a cascade of demethylation via ATF3 recruited TET1, followed by increased RNA PolII pause via CTCF at the intron 9a leads to inclusion of exon 9a. The P4HA1 9a isoform leads to enhanced invasion under hypoxic conditions by increasing deposition of collagen in the ECM. These results provide a novel hypoxia-induced HIF1ɑ-ATF3-P4HA1 axis which can be potentially exploited as a therapeutic target to impede EMT and ultimately breast cancer invasion.

2024-12-31 | GSE274936 | GEO

Hypoxia induced ATF3 escalates breast cancer invasion by increasing collagen deposition

Project description:Hypoxia induced ATF3 escalates breast cancer invasion by increasing collagen deposition

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Long-term exposure of early-transformed human mammary cells to low-doses of Benzo[a]pyrene and/or Bisphenol-A enhances their cancerous phenotype via an AhR/GPR30 interplay

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