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Enhanced Collagen Secretion in Epithelial Cancer Cells is associated with L1CAM Deficiency

ABSTRACT: Enhanced Collagen Secretion in Epithelial Cancer Cells is associated with L1CAM Deficiency

PROVIDER: PRJNA1119495 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29268965_1.fastq.gz	Fastqsanger.gz
	SRR29268965_2.fastq.gz	Fastqsanger.gz
	SRR29268966_1.fastq.gz	Fastqsanger.gz
	SRR29268966_2.fastq.gz	Fastqsanger.gz
	SRR29268967_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Enhanced Collagen Secretion in Epithelial Cancer Cells is associated with L1CAM Deficiency

Project description:Collagen, a critical component of the tumor microenvironment (TME), significantly influences cancer-associated fibrosis, tissue stiffness, immune response, and metastasis. Pancreatic ductal adenocarcinoma (PDAC) is characterized by excessive collagen deposition, and effective therapies remain limited. Our research challenges conventional understanding by highlighting the remarkable ability of specific tumor epithelial populations, particularly those with low levels of L1 cell adhesion molecule (L1CAM) expression (L1low), to actively modulate collagen dynamics within the TME. Transcriptome analysis of PDAC cells with varying L1 expression reveals shifts in collagen-related pathways, with heightened expression of collagen 17A1 (COL17A1) in L1low cells. Alongside, L1low cells exhibit enhanced migratory capacity. In an orthotopic mouse model, L1low cancer cells demonstrate increased collagen deposition, resistance to gemcitabine treatment, and an elevated propensity for liver metastases. Treatment with Tranilast, an anti-fibrotic drug, significantly reduces tumor volume and collagen deposition while enhancing L1 expression. This, in turn, mitigates tumor invasiveness and suppresses metastases formation. Overall, our study uncovers a novel role for L1CAM in PDAC aggressiveness and fibrosis, revealing a new epithelial population capable of collagen secretion and challenging the traditional notion that this function is solely attributed to stromal cells.

2024-06-11 | GSE268948 | GEO

Type VI Collagen Deficiency Causes Enhanced Periodontal Tissue Destruction in Induced Periodontitis

Project description:Type VI Collagen Deficiency Causes Enhanced Periodontal Tissue Destruction in Induced Periodontitis

| PRJNA1076178 | ENA

Type VI Collagen Deficiency Causes Enhanced Periodontal Tissue Destruction in Induced Periodontitis

Project description:Single cell analysis of PDL cells in ligature-induced periodontitis: The periodontal ligament (PDL) is a fibrillar connective tissue that lies between the alveolar bone and the tooth and is composed of highly specialized extracellular matrix (ECM) molecules and a heterogeneous population of cells that are responsible for collagen formation, immune response, bone formation, and chewing force sensation. Type VI collagen (COL6), a widely distributed ECM molecule, plays a critical role in the structural integrity and mechanical properties of various tissues including muscle, tendon, bone, cartilage, and skin. However, its role in the PDL remains largely unknown. Our study shows that deficiency of COL6 impairs PDL fibrogenesis and exacerbates tissue destruction in ligature-induced periodontitis (LIP). We found that COL6 deficient mice exhibited increased bone loss and degraded PDL in LIP and that fibroblasts expressing high levels of Col6α2 are pivotal in ECM organization and cell-ECM interactions. Moreover, COL6 deficiency in the PDL led to an increased number of fibroblasts geared towards the inflammatory response. We also observed that cultured COL6 deficient fibroblasts from the PDL exhibited decreased expression of genes related to collagen fiber metabolism and ECM organization, and migration and proliferation. Our findings suggest that COL6 plays a crucial role in the PDL, influencing fibroblast function in fibrogenesis and affecting the immune response in periodontitis. These insights could advance our understanding of the molecular mechanisms underlying PDL maturation and periodontal disease.

2024-06-24 | GSE255695 | GEO

Cyclophilin B deficiency causes abnormal dentin collagen matrix

Project description:To evaluate the effects of cyclophilin B deficiency on expression levels of collagen family members in dentin, we performed protein identification of cyclophilin B-WT, -Het, and -KO teeth after trypsin digestion.

2017-07-20 | PXD006021 | JPOST Repository

L1CAM knockdown significantly reduces metastasis in a xenograft model of human melanoma

Project description:As L1CAM expression is associated with metastasis in melanoma patients, it could be a target for the combination therapies. We investigated the functional role of L1CAM in melanoma metastasis by the use of a xenograft model of human melanoma in mice using RNAi mediated L1CAM knockdown melanoma cells.

2016-07-27 | GSE84864 | GEO

XBP1s-Mediated Endoplasmic Reticulum Proteostasis Network Enhancement Can Selectively Improve Folding and Secretion of an Osteogenesis Imperfecta-Causing Collagen-I Variant

Project description:Osteogenesis imperfecta (OI) is most commonly caused by autosomal dominant mutations in genes encoding collagen type-I. Here, we test the hypothesis that modulation of the endoplasmic reticulum (ER) proteostasis network via the unfolded protein response (UPR) can improve the folding and secretion of the lethal osteogenesis imperfecta (OI)-causing G425S a1(I) variant. We show that specific induction of the UPR’s XBP1s transcriptional response enhances G425S a1(I) secretion up to ~300% of basal levels. Notably, the effect is selective – WT a1(I) secretion is unaltered by XBP1s. XBP1s pathway activation appears to post-translationally enhance the folding/assembly and secretion of G425S a1(I). Consistent with this notion, we find that the stable, triple-helical collagen-I secreted by XBP1s-activated G425S a1(I) patient fibroblasts includes a higher proportion of the mutant a1(I) polypeptide than the collagen-I secreted under basal ER proteostasis conditions.

2023-12-19 | GSE163812 | GEO

Transcription profiling of human Hep3B cells transfected with L1CAM

Project description:To compare the transcription profiling between empty vector transfected Hep3B and L1CAM transfected Hep3B

2011-08-01 | E-MEXP-1357 | biostudies-arrayexpress

L1CAM dependent transcriptional programs in brain metastatic cells

Project description:L1CAM dependent gene expression programs in vitro and ex vivo were analyzed by translating ribosome affinity purification and sequencing (TRAP-Seq).

2018-07-23 | GSE82281 | GEO

A Novel Silent Mutation in the L1CAM Gene causing Fetal Hydrocephalus

Project description:To explore the genetic cause of a Chinese woman with fetal hydrocephalus X-linked hydrocephalus (XLH), a genetic disorder, has an incidence of 1/30,000 male births. The great proportion of XLH is ascribed to loss of function mutations of L1 cell adhesion molecule gene (L1CAM), but silent mutations in L1CAM with pathogenic potential were rare, and were usually ignored especially in WES detection. In the present study, we describe a novel silent L1CAM mutation in a Chinese pregnant woman reporting continuous five times pregnancies with fetal hydrocephalus. After fetal blood sampling, we found c.453G>T (p.Gly151=) in L1CAM gene of the fetus by whole exome sequencing (WES), RT-PCR of the mRNA from cord blood mononuclear cells and subsequent sequence analysis identified the mutation created a potential 5' splice site consensus sequence, which would result in an in-frame deletion of 72 bp from exon 5 and 24 amino acids of the L1CAM protein. Heterozygous mutations were confirmed in analyzing DNA and mRNA from peripheral blood mononuclear cells of the woman, and, a severe L1 syndrome was confirmed by fetal ultrasound scan and MRI. Our study first indicated c.453G>T (p.Gly151=) in L1CAM could be disease causing for hydrocephalus, which would aid in genetic counseling for the prenatal diagnosis of hydrocephalus. Meanwhile, it suggested some silent mutations detected in WES should not be ignored, splicing predictions of these mutations were necessary.

2019-07-16 | GSE133063 | GEO

L1CAM is a marker for isolating corticospinal motor neurons in the developing brain

Project description:The cerebral cortical tissue of murine embryo and pluripotent stem cell-derived neurons can survive in adult brain and extend axons to the spinal cord. These features suggest that cell transplantation can be a strategy to reconstruct the corticospinal tract (CST). It is unknown, however, which cell population makes for safe and effective donor cells. To address this issue, we grafted the cerebral cortex of E14.5 mouse to the brain of adult mouse and found that the cells in the graft extending axons along the CST expressed CTIP2. By using CTIP2:GFP knockin mouse embryonic stem cells, we identified L1CAM as a cell surface marker to enrich CTIP2+ cells. We sorted L1CAM+ cells from E14.5 mouse brain and confirmed that they extended a larger number of axons along the CST compared to L1CAM- cells. Our results suggest that sorting L1CAM+ cells from the embryonic cerebral cortex enriches subcortical projection neurons to reconstruct the CST.

2020-02-29 | GSE132362 | GEO

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