Abstract
BackgroundLong noncoding RNA (lncRNA) LINC00922 has been reported to promote tumorigenesis of lung and breast cancer. However, the functions and mechanisms of LINC00922 in ovarian cancer (OC) remain unclarified. The current study aims to clarify the detailed functions and underlying mechanisms of LINC00922 in the progression of OC.MethodsLINC00922 expression in OC tissues and cells was identified by a comprehensive strategy of data miming, computational biology and quantitative real-time polymerase chain reaction (RT-qPCR) experiment. In vitro CCK-8, wound healing, transwell invasion, western blotting and in vivo tumorigenesis assays LINC00922 were conducted to evaluate the functions of LINC00992. Subsequently, bioinformatics technology and dual luciferase reporter assay were performed to confirm the between miR-361-3p and LINC00922 or CLDN1. Finally, rescue experiments were performed to confirm whether LINC00922 effect functions of OC cells through regulation of miR-361-3p.ResultsLINC00922 was significantly upregulated in OC tissues and cell lines, which is significantly positively corelated with the poor prognosis of patients with OC. LINC00922 knockdown inhibited proliferation and tumorigenesis of OC cells in vitro and vivo. In addition, LINC00922 knockdown suppressed migration, invasion, and EMT of OC cells in vitro. Mechanically, LINC00922 could competitively bind with miR-361-3p to relieve the repressive effect of miR-361-3p on its target gene CLDN1 in OC cells. In addition, silencing miR-361-3p promoted OC cell proliferation, migration, invasion, EMT and Wnt/β-catenin signaling, while LINC00922 knockdown inhibited Wnt/β-catenin signaling by upregulating miR-361-3p. Rescue experiments revealed that LINC00922 knockdown inhibited OC cell proliferation, migration, invasion and EMT by regulating miR-361-3p.ConclusionThis study suggested that LINC00922 could competitively bind with miR-361-3p to promote the CLDN1 expression and activate Wnt/β-catenin signaling in OC progression, which providing a promising therapeutically target for OC.
Highlights
Ovarian cancer (OC), a frequently prevalent malignant tumor, is the primary cause of cancer-related death in women worldwide [1, 2]
LINC00922 is upregulated in ovarian cancer and correlated with poor prognosis We initially identified the critical Long noncoding RNA (lncRNA) regulating OC progression based on GSE74448 and TCGA/GETx OC data sets
Combined differential expression and survival analysis, we found that DANT2, LINC01711, and LINC00922 were significantly upregulated in OC tissues and positively correlated with poor prognosis of patients with OC
Summary
Ovarian cancer (OC), a frequently prevalent malignant tumor, is the primary cause of cancer-related death in women worldwide [1, 2]. In the United States, 21, 750 new cases of OC are reported in 2020. Around 13, 940 mortalities were reported annually [1]. With advancements in the field of oncology diagnosis in the last decade, a 5-year survival rate of patients with OC has increased by approximately 90% [3]. Clinical outcomes of patients with advanced OC remain unfavorable, with less than 6% of the 5-year survival rate [4]. Long noncoding RNA (lncRNA) LINC00922 has been reported to promote tumorigenesis of lung and breast cancer. The functions and mechanisms of LINC00922 in ovarian cancer (OC) remain unclarified. The current study aims to clarify the detailed functions and underlying mechanisms of LINC00922 in the progression of OC
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