GSE174741
LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line
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. Overall design: We compared gene expression in the 12Z endometrial endometriosis cell line between 3 control samples (non-targeting siRNA oligo, Cat. 4390846, Ambion, USA)  and 3 LINC01133 knockdown samples (Cat. S444575)