Expression data from Periostin isoform 3 and 6 overexpressing oral cancer cells
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ABSTRACT:
PROVIDER: PRJNA517802 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The aim to the study was to elucidate the character of Periostin isoform 3 and 6 by carrying out a geome-wide expression analysis.
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Project description:Periostin participates in different processes involved in connective tissue homeostasis. It is also involved in repairment of damaged tissues. We used the osteoblast murine cell line MC3T3-E1 cell line to show how overexpresion of periostin is able to increase their adhesion properties while diminishing their migration capacity. By differential gene expression we evaluated putative targets involved in those cellular properties.
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Project description:We compared transcriptional differences between Periostin siRNA treated and GFP-siRNA treated in OP9 cells using Affymetrix mouse 430_2 array.
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Project description:Cancer cell dissemination to sentinel lymph nodes associates with poor patient outcomes, particularly in breast cancer. The process by which cancer cells egress from the primary tumor upon interfacing with the lymphatic vasculature is complex and driven by dynamic interactions between cancer cells and stromal cells, including cancer associated fibroblasts (CAFs). The matricellular protein periostin can distinguish CAF subtypes in breast cancer and is associated with increased desmoplasia and disease recurrence in patients. However, since periostin is secreted, periostin-expressing CAFs are difficult to characterize in situ, limiting our understanding of their specific contribution to cancer progression. Here, we used in vivo genetic labeling and ablation to lineage trace periostin+ cells and characterize their functions during tumor growth and metastasis. Periostin-expressing CAFs were spatially found at periductal and perivascular margins, were enriched at lymphatic vessel peripheries, and were differentially activated by highly-metastatic cancer cells versus poorly-metastatic counterparts. Surprisingly, genetically depleting periostin+ CAFs slightly accelerated primary tumor growth but impaired intratumoral collagen organization and inhibited lymphatic, but not lung, metastases. Periostin ablation in CAFs impaired their ability to deposit aligned collagen matrices and inhibited cancer cell invasion through collagen and across lymphatic endothelial cell monolayers. Thus, highly-metastatic cancer cells mobilize periostin-expressing CAFs in the primary tumor site that promote collagen remodeling and collective cell invasion within lymphatic vessels and ultimately to sentinel lymph nodes.
2023-05-03 | GSE231594 | GEO
Project description:The endoplasmic reticulum (ER) is the site of secretory lipoprotein production and de novo cholesterol synthesis, yet little is known about how these activities are coordinated with each other, or with the activity of the COPII machinery, which transports ER cargo to the Golgi. The Sar1B component of this machinery is mutated in Chylomicron Retention Disorder, establishing that this Sar1 isoform secures delivery of dietary lipids into the circulation. We used microarrays to investigate the effect of overexpression of Sar1 isoforms and a constitutively active mutant form of Sar1B, Sar1B:H79G, on global gene expression in rat hepatoma cell line, McArdle RH7777 and identified a strong down-regulation of cholesterol biosynthetic gene mRNA expression in the Sar1B:H79G-, but not the wild-type Sar1A- or Sar1B-overexpressing cell lines. RNA was extracted from cell cultures of control McArdle RH7777, and transgenic lines overexpressing human Sar1-isoforms: one for Sar1A, two for Sar1B and two expressing a constitutively active mutant form of Sar1B, Sar1B:H79G, that cannot complete GTP hydrolysis, and hybridized on Affymetrix GeneChip Rat Genome 230 2.0 arrays.
2013-12-16 | E-GEOD-52969 | biostudies-arrayexpress
Project description:Cancer cell dissemination to sentinel lymph nodes associates with poor patient outcomes, particularly in breast cancer. The process by which cancer cells egress from the primary tumor upon interfacing with the lymphatic vasculature is complex and driven by dynamic interactions between cancer cells and stromal cells, including cancer associated fibroblasts (CAFs). The matricellular protein periostin can distinguish CAF subtypes in breast cancer and is associated with increased desmoplasia and disease recurrence in patients. However, since periostin is secreted, periostin-expressing CAFs are difficult to characterize in situ, limiting our understanding of their specific contribution to cancer progression. Here, we used in vivo genetic labeling and ablation to lineage trace periostin+ cells and characterize their functions during tumor growth and metastasis. Periostin-expressing CAFs were spatially found at periductal and perivascular margins, were enriched at lymphatic vessel peripheries, and were differentially activated by highly-metastatic cancer cells versus poorly-metastatic counterparts. Surprisingly, genetically depleting periostin+ CAFs slightly accelerated primary tumor growth but impaired intratumoral collagen organization and inhibited lymphatic, but not lung, metastases. Periostin ablation in CAFs impaired their ability to deposit aligned collagen matrices and inhibited cancer cell invasion through collagen and across lymphatic endothelial cell monolayers. Thus, highly-metastatic cancer cells mobilize periostin-expressing CAFs in the primary tumor site that promote collagen remodeling and collective cell invasion within lymphatic vessels and ultimately to sentinel lymph nodes.
2023-05-05 | GSE231806 | GEO
Project description:Periostin is a matricellular protein encoded by the POSTN gene that is alternatively spliced to produce ten different isoforms of periostin with a molecular weight ranging from 78 to 91 kDa. Periostin is known to promote fibrillogenesis, organize the extracellular matrix, and bind integrin-receptors to induce cell signaling. Periostin is a key component of the wound healing process but is also known to participate in the pathogenesis of different diseases including atopic dermatitis, asthma, and cancer. In both health and disease, the functions of the different periostin isoforms are largely unknown. The ability to precisely determine the isoform profile of a given human sample is fundamental for characterizing their functional significance. Identification of periostin isoforms is most often carried out at the transcriptional level using RT-PCR based approaches. Though, it must be recognized that periostin exerts it functions at the translational level and is an extracellular protein making it impossible to derive transcriptional information for e.g. plasma periostin that is spatially disconnected from the cell it was expressed by. Consequently, monitoring periostin isoforms at the protein level is highly advantageous. In the publication connected to this dataset we present a fully developed top down mass spectrometry assay for identification and quantification of periostin splice isoforms from any human sample at the protein level.
2024-06-11 | PXD045560 | Pride
Project description:The endoplasmic reticulum (ER) is the site of secretory lipoprotein production and de novo cholesterol synthesis, yet little is known about how these activities are coordinated with each other, or with the activity of the COPII machinery, which transports ER cargo to the Golgi. The Sar1B component of this machinery is mutated in Chylomicron Retention Disorder, establishing that this Sar1 isoform secures delivery of dietary lipids into the circulation. We used microarrays to investigate the effect of overexpression of Sar1 isoforms and a constitutively active mutant form of Sar1B, Sar1B:H79G, on global gene expression in rat hepatoma cell line, McArdle RH7777 and identified a strong down-regulation of cholesterol biosynthetic gene mRNA expression in the Sar1B:H79G-, but not the wild-type Sar1A- or Sar1B-overexpressing cell lines.
2013-12-16 | GSE52969 | GEO
Project description:Periostin, a matricellular protein, has been reported to be important in supporting tumor cell dissemination. However, the molecular mechanisms underlying periostin function within the tumor microenvironment are poorly understood. In this study, we observe that loss of periostin decreases esophageal squamous cell carcinoma (ESCC) tumor growth in vivo and demonstrate that periostin cooperates with a conformational missense p53 mutation to enhance invasion. Pathway analyses reveal that invasive esophageal cells expressing periostin and p53R175H mutation display activation of signal transducer and activator of transcription 1 (STAT1) target genes, suggesting that the induction of STAT1 and STAT1-related genes could foster a permissive microenvironment that facilitates invasion of esophageal epithelial cells into the extracellular matrix (ECM). Genetic knockdown of STAT1 in transformed esophageal epithelial cells underscores the importance of STAT1 in promoting invasion and potentiate tumor resistance to genotoxic stress. Furthermore, we find that STAT1 is activated in ESCC xenograft tumors but this activation is attenuated with inducible knockdown of periostin in ESCC tumors. Overall, these results highlight the molecular mechanisms supporting the capacity of periostin in mediating tumor invasion during ESCC development. Pre-clinical study hTERT: EPC cells immortalized by expression of hTERT hTERT_p53: EPC cells expressing hTERT and mutant P53 hTERT_p53_POSTN: EPC cells expressing hTERT, mutant P53, and POSTN.
2016-06-01 | E-GEOD-48999 | biostudies-arrayexpress