Epithelial-mesenchymal transition (EMT) plays a significant part in the pathogenesis of endometriosis by facilitating the migration and invasion abilities of cells. Integrin-linked kinase (ILK) increases the cell migration and invasion abilities by inducing the EMT. Eutopic and control endometrial stromal cells (EuSCs and CSCs) were isolated and cultured. Cell migration and invasion abilities were detected by transwell assays. Levels of proteins were detected by Western blot. EuSCs showed higher levels of ILK, N-cadherin, vimentin and stronger migration and invasion abilities. After transfection of siRNA-ILK, E-cadherin and keratin levels were increased while N-cadherin and vimentin levels were decreased in EuSCs. Besides that, the migration and invasion abilities of EuSCs were significantly decreased after transfection of siRNA-ILK. On the contrary, levels of ILK, N-cadherin and vimentin were increased while levels of E-cadherin and keratin were decreased simultaneously after transfecting CSCs with pEGFP-C1-ILK. Simultaneously, the migration and invasion abilities of CSCs were increased after transfection of pEGFP-C1-ILK. Our study verified that high expression of ILK enhanced the migration and invasion abilities of ESCs by facilitating the EMT. Given that ILK played crucial roles in the pathogenesis of endometriosis, it may be considered as a promising targeted therapy for endometriosis.
Objective: MicroRNAs (miRNAs) are highly involved in cancer development, including in cervical cancer (CC). In this study, we aimed to investigate the role and possible mechanism of a poorly studied miRNA, miR-1193, in CC progression. Materials and Methods: Expression of miR-1193 was determined in 60 pairs of cervical samples. The impacts of miR-1193 on CC cell proliferation, invasion and migration capacities were verified by CCK-8, transwell and wound healing assays, respectively. Then, bioinformatics prediction, luciferase reporter assay, qRT-PCR and Western blot were successively conducted to study the targeting of claudin 7 (CLDN7) by miR-1193. After CLDN7 was restored in miR-1193-overexpressed cells, the rescue effects were determined. Finally, CLDN7 expression was analyzed in cervical samples, and its expression correlation with miR-1193 was explored. Results: Compared with paired normal tissues, miR-1193 was sharply decreased in abnormal tissues (intraepithelial lesions and cancerous tissues). Especially, miR-1193 expression was gradually decreased in low-grade squamous intraepithelial lesions, high-grade squamous intraepithelial lesions and CC. Enforced expression of miR-1193 inhibited CC cell proliferation, invasion and migration. Mechanistically, we confirmed CLDN7 as a target of miR-1193, and restoration of CLDN7 robustly rescued the tumor suppressing effects of miR-1193 in CC cells. CLDN7 was upregulated in abnormal cervical tissues and its expression exhibited inverse correlation with that of miR-1193 in CC. Conclusion: Our results suggested that miR-1193 exerted tumor inhibitory roles in CC malignancy by directly targeting CLDN7.
Endometriosis is a common benign disease in gynecology and has malignant biological behaviors, such as hyperplasia, invasion, metastasis, and recurrence. However, the pathogenesis of endometriosis remains unclear. The present study aimed to investigate whether LncRNA HOTAIR regulates cell invasion and migration in endometriosis by regulating the miR-519b-3p/PRRG4 pathway. The qRT-PCR results showed that the average relative expression of LncRNA HOTAIR was much higher in ectopic endometrial tissues than in eutopic endometrial tissues. Scratch and transwell assays showed that the cell migration and invasion ability of LncRNA HOTAIR overexpression group was significantly higher than those in the control group. Conversely, the LncRNA HOTAIR knockdown group showed the opposite results. Bioinformatics analysis suggested that the downstream target genes of LncRNA HOTAIR were miR-519b-3p and Prrg4. Knockdown of LncRNA HOTAIR can reduce the up-regulation of Prrg4 by miR-519b-3p and then inhibit the invasion and migration ability of endometrial stromal cells. In Conclusion, LncRNA HOTAIR can regulate the ability of invasion and migration of endometrial stromal cells, and its mechanism is proved by regulating the miR-519b-3p/PRRG4 pathway.
Occludin protein may contribute to the development of cervical cancer. However, it was not correlated with the clinical features.
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