Role of mucin MUC5AC on tumor angiogenesis and lung adenocarcinoma development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1228070 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32484338.fastq.gz | Fastqsanger.gz | |||
| SRR32484339.fastq.gz | Fastqsanger.gz | |||
| SRR32484340.fastq.gz | Fastqsanger.gz | |||
| SRR32484341.fastq.gz | Fastqsanger.gz | |||
| SRR32484342.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:MUC5AC is a secretory type of mucin, which is significantly overexpressed in lung adenocarcinoma and associated with poor survival outcomes. Expression of MUC5AC and its sialylation is required for alteration of tumor matrix remodeling through interacting with integrin β4 in lung adenocarcinoma. We have previously shown that sialylated MUC5AC is required for lung adenocarcinoma cell growth and metastasis. To understand the molecular mechanism of MUC5AC in lung adenocarcinoma development, we performed RNA sequence analysis using MUC5AC knockdown cells (A549-shMUC5AC) and scramble cells (A549-shRNA). We observed that several tumor matrix proteins including VCAN and integrin β4 were significantly downregulated and are associated with tumor angiogenesis. In this study, we reported that sialylated MUC5AC induces tumor angiogenesis by altering tumor matrix protein VCAN during lung adenocarcinoma development and metastasis.
2025-04-15 | GSE290456 | GEO
Project description:Tumors are prone to immune escape by developing strategies to evade immunity. ST6GalNAc-I is an O-glycosyltransferase, which catalyzes the addition of sialic acid onto the first sugar GalNAc (Tn) and results in the formation of Neu5Acα2, 6GalNAc (STn) carbohydrate antigen. SialylTn plays an important role in tumor progression, angiogenesis, and metastasis. RNA sequence analysis was performed using genetically engineered LUAD mouse model tumors (KrasG12D/+; Trp53R172H/+; Ad-Cre (KPA) and KrasG12D/+; Ad-Cre (KA)). We have performed RNA sequence analysis using KPA tumors (N=3), KA tumors (N=3), and littermate control lung tissues (N=3). In comparison to normal lung tissues, several genes were significantly overexpressed in KPA and KA-derived LUAD tumors, including Meg3, Slc7a5, Cxcr1, Awat1, Kng2, Gjb3, Mfi2, and Dlk1. More specifically, St6galnac-I was significantly overexpressed in aggressive-type KPA tumor tissues compared to KA and normal lung tissues. Expression of ST6GalNAc-I is associated with tumor progression and angiogenesis by immunosuppression. Mechanistically, ST6GalNAc-I promotes tumor cell sialylation that impacts tumor angiogenesis by altering mucin MUC5AC. Similarly, ST6GalNAc-I regulates Nectin2 sialylation which leads to immunosuppression and tumor progression. Overall, our study defined that ST6GalNAc-I is a critical molecule for tumor cell sialylation for disease aggressiveness.
2025-04-15 | GSE290957 | GEO
Project description:Role of ST6GalNAc-I in immunosuppression and lung adenocarcinoma development
| PRJNA1231076 | ENA
Project description:Unveiling the role of RAB13 localisation in angiogenesis
| PRJNA649779 | ENA
Project description:Role of Hdac2 in pancreatic ductal adenocarcinoma
| PRJNA604969 | ENA
Project description:While growing in the human intestine, C. jejuni grows within the mucus layer. The largest constituents of this layer are the large mucin glycoproteins. A transcriptomic profile of C. jejuni NCTC11168 growing in a mucin-containing minimal medium seeks to describe the effect of the presence of mucin proteins on the transcriptome of C. jejuni. Microarray data was collected from three independent biological replicates and 9 technical replicates for each biological replicate.
2011-04-01 | E-GEOD-28295 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) originates from normal pancreatic ducts where digestive juice is regularly produced. It remains unclear how PDAC can escape auto-digestion by digestive enzymes. Here we show that human PDAC tumor cells use gasdermin E (GSDME), a pore-forming protein upon caspase 3 cleavage, to mediate the digestive resistance. We find that GSDME facilitates the expression of mucins 1 and 13 in pancreatic tumor cells, which forms a barrier to prevent chymotrypsin-mediated destruction. Inoculation of GSDME-/- PDAC cells results in subcutaneous but not orthotopic tumor formation in mice. Either inhibiting or knocking out MUC1 or MUC13 abrogates orthotopic PDAC growth in NOD-SCID mice. Mechanistically, GSDME interacts with and transports transcription factor YBX1 into the nucleus where YBX1 directly promotes mucin expression. This GSDME-YBX1-mucin axis is also confirmed in PDAC patients. These findings uncover a unique survival mechanism of PDAC cells in pancreatic microenvironments, thus providing a potential target for PDAC treatment.
2022-05-20 | PXD030879 | Pride
Project description:While growing in the human intestine, C. jejuni grows within the mucus layer. The largest constituents of this layer are the large mucin glycoproteins. A transcriptomic profile of C. jejuni NCTC11168 growing in a mucin-containing minimal medium seeks to describe the effect of the presence of mucin proteins on the transcriptome of C. jejuni.
2011-04-01 | GSE28295 | GEO
Project description:A growing body of literature has proposed cell-autonomous tumor suppressor functions for the mir-143~145 cluster in a variety of human cancers, including lung adenocarcinoma, and has reported therapeutic benefits of delivering mir-143 and mir- 145 to tumors. In contrast to these studies, we found that depletion or forced expression of mir-143 and mir-145 in an autochthonous mouse model of lung adenocarcinoma did not affect tumor development. Surprisingly, we observed that loss of mir-143~145 from the tumor microenvironment significantly reduced tumor burden, indicating a non-cell- autonomous role for these miRNAs in promoting tumorigenesis. By examining the expression patterns of different cell populations isolated in vivo from tumor-bearing lungs using an integrated computational approach, we identified a role for mir-145 in stimulating the proliferation of endothelial cells by downregulating an inhibitory kinase, Camk1d, which prevents mitotic entry. As a consequence, tumors in mir-143~145- deficient animals exhibited diminished hallmarks of neo-angiogenesis, increased apoptosis and their expansion appeared limited by the tumor’s ability to co-opt the alveolar vasculature. These findings show that expression of the mir-143~145 cluster in the tumor stroma promotes rather than suppresses tumorigenesis and cautions against the use of these miRNAs as agents in cancer therapeutics.
2016-05-21 | GSE71877 | GEO
Project description:MicroRNAs (miRNAs) are small non-coding RNAs that act as post-transcriptional gene modulators. Ginsenoside-Rg1, one of the active components of ginseng, has been confirmed by us as an angiogenesis inducer. Using miRNA microarray analysis, a total of 15 (including miR-214) and 3 miRNAs were found to be down- or up-regulated by Rg1 in human umbilical vein endothelial cells (HUVEC), respectively. Since miR-214 is closely related to endothelial nitric oxide synthase (eNOS) and hence angiogenesis; its expression was further validated by qRT-PCR. We also investigated the role of miR-214 on eNOS expression and in tubulogenesis of HUVEC by transfection of specific miRNA inhibitor or precursor. Our results suggested that Rg1 can down-regulate miR-214 expression in HUVEC, leading to an increase in eNOS expression which can promote angiogenesis. This result signifies a new understanding towards how a simple natural compound can affect physiological changes through modulation of miRNA expression. The study is used to investigate the role of miRNA-214 in Rg1-induced human endothelial cells.
2010-08-05 | E-GEOD-17541 | biostudies-arrayexpress