LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA731387 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14599984_1.fastq.gz | Fastqsanger.gz | |||
| SRR14599984_2.fastq.gz | Fastqsanger.gz | |||
| SRR14599985_1.fastq.gz | Fastqsanger.gz | |||
| SRR14599985_2.fastq.gz | Fastqsanger.gz | |||
| SRR14599986_1.fastq.gz | Fastqsanger.gz |
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Project description:Endometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and associated with chronic pain and infertility. We investigated the role of LINC01133 in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriosis lesions. As expression appeared higher in the epithelial endometrial layer, we performed an siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells. Gene ontology analysis of differentially expressed genes detected by RNA sequencing indicated that cell proliferation and migration pathways were affected in line with the observed phenotype. We validated upregulation of p21 and downregulation of cyclin at the protein level, which together with DNA FACS analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle progression. Further, we validated upregulation of the protein kinase TESK1 at the protein level, and found a corresponding increased phosphorylation and therefore inactivation of the actin severing protein Cofilin, which may explain changes in the cytoskeleton and cellular migration. These results indicate that LINC01133 upregulation is associated with endometriosis, which may be due to its effects on genes involved in the cellular proliferation and migration pathways.
2021-08-23 | GSE174741 | GEO
Project description:Endometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and is associated with chronic pain and infertility. We investigated the role of the long intergenic noncoding RNA 01133 (LINC01133) in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriotic lesions. As expression appeared higher in the epithelial endometrial layer, we performed a siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells. Gene ontology analysis of differentially expressed genes indicated that cell proliferation and migration pathways were affected in line with the observed phenotype. We validated upregulation of p21 and downregulation of Cyclin A at the protein level, which together with the quantification of the DNA content using fluorescence-activated cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle. Further, we found testis-specific protein kinase 1 (TESK1) kinase upregulation corresponding with phosphorylation and inactivation of actin severing protein Cofilin, which could explain changes in the cytoskeleton and cellular migration. These results indicate that endometriosis is associated with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation and migration pathways.
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Project description:MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53
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Project description:The long intergenic non-coding RNA linc01133 is reported to be oncogenic in various malignancies. However, the role and mechanism of linc01133 in regulating gastric cancer growth is still not clear. In the present study, we found that linc01133 was significantly up-regulated in gastric cancer tissues compared to non-tumorous gastric tissues. Linc01133 over-expression significantly correlated with tumor size and tumor differentiation in gastric cancer patients. The expression of linc01133 was regulated by c-Jun and c-Fos collaboratively. In both in vitro and in vivo studies, linc01133 was shown to promote gastric cancer cell growth. Linc01133 localized in the cytoplasm and functioned as an endogenous competing RNA of miR-145-5p to up-regulate the expression of YES1，which was proved to be the target gene of miR-145-5p. By promoting YES1-dependent YAP1 nuclear translocation, linc01133 up-regulated the expression of the key cell cycle regulators CDK4, CDK6 and cyclin D1 to promote G1-S phase transition. Thus, our study unveiled the function and mechanism of linc01133 regulating cell cycle progression in gastric cancer.
2021-12-21 | GSE191227 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited treatment methods. Long non-coding RNAs (lncRNAs) have been found involved in tumorigenic and progression. The present study revealed that LINC01133, a fewly reported lncRNA, was one of 16 hub genes that could predict PDAC patients' prognosis. LINC01133 was over-expressed in PDAC tumors compared to adjacent pancreas, and could promote PDAC proliferation and metastasis in vitro and in vivo, as well as inhibited PDAC apoptosis. LINC01133 expression positively correlated to secreted phosphoprotein 1 (SPP1) expression, leading to an enhanced epithelial-mesenchymal transition (EMT) process. LINC01133 bound with actin-related protein 3 (Arp3), the complex reduced SPP1 mRNA degradation which increased SPP1 mRNA level, ultimately leading to PDAC proliferation. This research revealed a novel mechanism of PDAC development and provided a potential prognosis indicator that may benefit PDAC patients.
2024-07-17 | GSE267702 | GEO
Project description:The PI3K pathway represents the most hyperactivated oncogenic pathway in triple-negative breast cancer (TNBC), a highly aggressive tumor subtype encompassing ~15% of breast cancers with no targeted therapeutics. Despite critical contributions of its signaling arms to disease pathogenesis, PI3K pathway inhibitors have not achieved expected clinical responses in TNBC owing largely to still-incomplete understanding of the compensatory cascades that operate downstream of PI3K. Here, we investigated the contributions of long non-coding RNAs (lncRNAs) to PI3K activities in clinical and experimental TNBC, and discovered a prominent role for LINC01133 as a PI3K-AKT signaling effector. We found that LINC01133 exerted pro-tumorigenic roles in TNBC, and that it governed a previously undescribed mTORC2-dependent pathway that activated AKT in a PI3K-independent manner. Mechanistically, we show that LINC01133 induced the expression of the mTORC2 component PROTOR1/PRR5 by competitively coupling away its negative mRNA regulator, the heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1). PROTOR1/PRR5 in turn was sufficient and necessary for LINC01133-triggered functions, casting previously unappreciated roles for this Rictor-binding protein in cellular signaling and growth. Notably, LINC01133 antagonism undermined cellular growth and we show that the LINC01133-PROTOR1/PRR5 pathway tightly associated with TNBC poor patient survival. Altogether, our findings uncovered a lncRNA-driven signaling shunt that acts as a critical determinant of malignancy downstream of the PI3K pathway and as a potential RNA-based theranostic in clinical TNBC management. We performed comparative gene expression profiling analyses using RNA-seq of triplicates of control 4T1 cells (harboring empty plasmid control) and 4T1 cell trioplicates expressing exogenous LINC01133.
2022-10-03 | GSE212004 | GEO
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Project description:We performed gene expression analysis human peritoneal endometriosis lesions, eutopic endometrium from endometriosis patients and peritoneum form endometriosis patients.The goal of the study was to analyse gene expression differences between peritoneal endometriosis lesion and eutopic endometrium and peritoneal endometriosis lesion and peritoneum.
2012-12-06 | E-MTAB-694 | biostudies-arrayexpress
Project description:This study explores how quercetin may treat endometriosis (EMs) by combining network pharmacology and transcriptome sequencing approaches. Through network pharmacology, 132 shared targets between quercetin and EMs were identified, with KEGG pathway analysis suggesting that the MAPK signaling pathway could be a significant therapeutic target. Transcriptome sequencing revealed that PDGFRB was highly expressed in ectopic endometrial tissue, a finding confirmed by immunohistochemistry (IHC) showing elevated levels of PDGFRB, RAS, RAF1, and ERK1/2 in ectopic lesions. In an EMs mouse model, quercetin treatment led to a marked reduction in ectopic lesion volume, lowered adhesion scores, and decreased expression of PDGFRB, RAS, RAF1, and ERK1/2 in endometrial tissues. Additionally, the knockdown of PDGFRB in endometriosis cells inhibited their proliferation, invasion, and migration, processes critical to EMs pathology. Quercetin treatment further suppressed cell viability and downregulated the protein expression of RAS, phosphorylated RAF1, RAF1, phosphorylated ERK, and ERK1/2. These findings collectively suggest that quercetin exerts its therapeutic effect in endometriosis by regulating the MAPK signaling pathway via PDGFRB, thereby reducing EMs cell proliferation, invasion, and migration. This study provides insights into quercetin’s multi-targeted mechanism of action in endometriosis treatment.
2024-11-16 | GSE281569 | GEO