Background: Ovarian cancer remains a leading cause of mortality in women. It is known that long non-coding RNA (lncRNA) controls various biological processes and pathogenesis of many diseases, including cancers. This study aimed to determine whether LINC00936 and microRNA-221-3p (miR-221-3p) influence the laminin alpha 3 chain gene (LAMA3) in the development of ovarian cancer. Methods: The expressions of LINC00936, miR-221-3p, and LAMA3 in ovarian cancer and adjacent tissues were assessed. Furthermore, ovarian cancer cells were transfected with vectors with overexpressed LINC00936, miR-221-3p mimic, miR-221-3p inhibitor, and si-LAMA3 to elucidate their functions in ovarian cancer cell proliferation, migration, invasion, angiogenesis, and tumorigenesis. The binding relationship between LINC00936 and miR-221-3p and the relationship between miR-221-3p and LAMA3 were verified to explore the mechanism of action of LINC00936 in ovarian cancer. LINC00936 binds to miR-221-3p as a ceRNA and regulates the expression of LAMA3. Results: LINC00936 and LAMA3 were poorly expressed, while miR-221-3p was highly expressed in ovarian cancer tissues. Over-expression of LINC00936 contributed to decreasing miR-221-3p expression and increasing LAMA3 expression. LINC00936 overexpression or miR-221-3p silencing downregulated the levels of PCNA, MMP-2, MMP-9, and VEGF and decreased cell proliferation, migration, invasion, angiogenesis, and ovarian cancer tumorigenesis. Conclusion: Collectively, overexpression of LINC00936 suppressed the development of ovarian cancer by competitively binding to miR-221-3p and controlling LAMA3 expression. These results could serve as a novel theoretical base for the treatment of ovarian cancer.
Early diagnosis of cervical cancer is essential for a good prognosis. Terahertz wave detection technology is a nondestructive and labelfree physical detection technology, which can detect and monitor the cancer cells in real time, especially for patients with deep or inaccessible tumors. In this study, a single-cell-layer microfluidic device was developed.After replacing the optical clearing agent, the characteristics of H8, HeLa and SiHa cell lines in adherent and suspended states were detected. Additionally, the absorption increased with increasing cell density. For the mixed suspension cell samples, principal component analysis-support vector machine method was used to identify benign and malignant cell component. After living cells formaldehyde, changes in cell membrane permeability were evaluated to identify the cell survival status (i.e., dead or living) based on terahertz spectroscopy amplitude differences. Therefore, extending the terahertz spectrum detection to the molecular level can characterize the life essence of cells and tissues.
Background: Ovarian cancer (OV) has been puzzling clinicians because of its poor prognosis. More and more evidence show that the G protein coupled receptor P2RY14 plays a key role in the initiation and progression of various types of human cancer. The purpose of our study is to explore the correlation between P2RY14 and the prognosis of ovarian cancer patients and the relevant mechanism.Methods: First, the differentially expressed gene P2RY14 was screened from The Cancer Genome Atlas (TCGA) database. Explored possible P2RY14 related miRNAs and lncRNAs through multiple public databases, predicted and analyzed the expression level of candidate miRNAs and candidate lncRNAs that can bind to candidate miRNAs in OV through StarBase database. The TIMER database was used to comprehensively analyze the expression of tumor infiltrating immune cells, and to analyze the correlation between the expression level of P2RY14 and the level of immune cell infiltration in OV or the expression level of immune checkpoints.Results: Patients with P2RY14 overexpression had better overall survival (OS) and progression-free interval (PFI). In the Targetscan database, 22 upstream miRNAs that may bind to P2RY14 were predicted.According to the regulatory network constructed by the Cytoscape software, correlation analysis and the role of miRNAs in the prognosis of OV, we first determined that the candidate miRNAs were miR-34c-5p.Then, we predicted the upstream lncRNAs of miR-34c-5p in the StarBase database, the expression level of these lncRNAs in OV in the Gene Expression Profiling Interactive Analysis (GEPIA) database, and the role in prognosis. We determined that LINC00665 is the most potential lncRNA upstream of ovarian cancer miRNA (hsa-miR-34c-5p)-P2RY14. Then, we analyzed the results in the Timer database, suggesting that P2RY14 expression was positively correlated with CD8 + T Cell, CD4 + T Cell, Macrophage, Neutral and Dendritic cells, and negatively correlated with B cells. Meanwhile, P2RY14 was positively correlated with CD274 and PDCD1.Conclusions: P2RY14 can be used as a new predictive biomarker of ovarian cancer. Intervention of P2RY14 can affect the prognosis of ovarian cancer by affecting LINC00665-miR-34c-5p-P2RY14 axis.These findings provide a potential target for the development of anti-cancer strategies for ovarian cancer.
Background: This study sought to analyze long non-coding ribonucleic acid (lncRNA) LINC00273 expression in ovarian cancer tissues, and to preliminarily explore its effect on the growth and invasion of ovarian cancer cells and its influencing mechanism. Methods: Quantitative real-time polymerase chain reaction was performed to detect the LINC00273 expression levels of cancerous ovarian tissues and their related cell lines. The ovarian cancer cells with the highest expression of LINC00273 were transfected with a knockdown lentiviral vector targeting the LINC00273 sequence and a negative control plasmid. The effects of the LINC00273 knockdown on the invasion and growth of these cancerous cells were evaluated by clonogenic assays, flow cytometry, EdU(5-Ethynyl-2'-deoxyuridine), Cell Counting Kit-8, and Transwell assays. Western Blot was used to measure the LINC00273 knockdown effects on invasion and migration-related gene expression, and the knockdown effects on the ovarian proliferation ability of the cancer cells in vivo were analyzed by in vivo nude mouse experiments.Results: LINC00273 expression was significantly more increased in the cancerous ovarian tissues than the adjacent tissues. The LINC00273 expression of the ovarian cancer cell lines was higher than that of the normal ovarian epithelial cells. LINC00273 knockdown greatly suppressed the proliferative and clonogenic function of these cancerous cells. The flow cytometry results revealed that LINC00273 knockdown notably induced G0/G1 phase arrest in the ovarian cancer cells. LINC00273 knockdown also promoted E-cadherin expression in the ovarian cancer cells, and inhibited vimentin, matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and N-cadherin, expression to inhibit the invasion and migration ability of the ovarian cancer cells. The in vivo experiments indicated that LINC00273 knockdown suppressed in vivo cancer cell proliferation in the ovaries.Conclusions: LINC00273 is highly expressed in both ovarian cancerous tissues and ovarian cancerous cell lines. LINC00273 knockdown greatly suppressed the proliferative and invasive capabilities of the cancerous ovarian cells. In terms of the molecular process, it may be that the knockdown of LINC00273 promotes E-cadherin and inhibits vimentin, N-cadherin, MMP-2, and MMP-9 expression in cancerous ovarian cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.