LncRNA ABCA9-AS1 as a ceRNA Promotes Gastric Cancer Progression by Sponging miR-497-5p to Regulate KIF23 Expression.

LncRNA ZNF582-AS1 Acts as a Tumor Suppressor in Endometrial Cancer via the miR-21-5p/miR-516a-3p/CREBRF Axis.

The ZNF582-AS1/miR-21-5p/miR-516a-3p/CREBRF regulatory axis provides mechanistic insights into EC tumorigenesis and emphasizes the tumor suppressive effect of ZNF582-AS1.

LncRNA SLC12A9-AS1 Drives Malignant Progression in Colorectal Cancer by Regulating miR-139-3p.

This study investigated the function of long noncoding RNA SLC12A9-AS1 in colorectal cancer (CRC) cells and its potential regulatory mechanism. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure SLC12A9-AS1 and miR-139-3p expression in CRC cell lines. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay, whereas migration and invasion were evaluated using permeable cell culture insert assays. The interaction between SLC12A9-AS1 and miR-139-3p was examined using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. SLC12A9-AS1 was significantly upregulated, whereas miR-139-3p was downregulated, in CRC cells. Silencing SLC12A9-AS1 markedly reduced cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT). The DLR and RIP assays supported an interaction between SLC12A9-AS1 and miR-139-3p. In addition, inhibition of miR-139-3p reversed the suppressive effects of SLC12A9-AS1 knockdown on malignant cellular phenotypes. Collectively, these findings indicate that SLC12A9-AS1 is abnormally overexpressed in CRC cells and that its knockdown attenuates malignant phenotypes, at least in part through regulation of miR-139-3p. These results provide new in vitro experimental evidence for understanding the molecular mechanisms involved in CRC pathogenesis.

LncRNA RASAL2-AS1 serves as a potential biomarker for prognosis and regulates cellular processes via the miR-590-5p/PDCD5 axis and Wnt/β-catenin pathway in cervical cancer

The objective of this research is to determine the relative abundances and clinical significance of the long non-coding RNA (lncRNA) RASAL2-AS1 in cervical cancer. Additionally, this study aims to elucidate its molecular mechanism in influencing malignant progression through the regulation of the microRNA-590-5p (miR-590-5p)/PDCD5 axis and the Wnt/β-catenin signaling pathway. Gene expression of RASAL2-AS1 was assessed in cervical cancer tissues ( n  = 103) using quantitative real-time PCR (qRT-PCR). The impacts on cellular events, epithelial-mesenchymal transition (EMT), and key signaling pathways were evaluated using CCK-8, Transwell, and Western Blot techniques. The target relationships among RASAL2-AS1, miR-590-5p, and PDCD5 were verified via luciferase reporter assays. RASAL2-AS1 exhibited significantly reduced expression in cervical cancer. Its downregulation was markedly associated with advanced FIGO staging ( P  = 0.014), lymph node metastasis ( P  = 0.035), and poor prognosis, establishing it as an independent indicator of unfavorable outcomes for cervical cancer patients (HR = 0.201, 95% CI = 0.087–0.464, P  < 0.001). Functionally, the upregulation of RASAL2-AS1 inhibited cervical cancer cell growth and EMT. Mechanistically, RASAL2-AS1 acted as a molecular sponge to sequester miR-590-5p, thereby alleviating its inhibitory effect on PDCD5. Furthermore, RASAL2-AS1 obstructs the Wnt/β-catenin pathway through the miR-590-5p/PDCD5 axis. RASAL2-AS1 exerts a tumor-suppressive effect in cervical cancer by functioning as a competing endogenous RNA (ceRNA) that modulates the miR-590-5p/PDCD5 axis and regulates the Wnt/β-catenin pathway.

Characterization of a novel lncRNA RP3-340N1.2 and its association with a miR-4650-5p/SHC1-related regulatory network in lung adenocarcinoma

Findings indicate that RP3-340N1.2 is aberrantly expressed in LUAD and may participate in tumor-associated cellular behaviors through a miR-4650-5p/SHC1-related regulatory mechanism.

LncRNA TRHDE-AS1 functions as a tumor suppressor in ovarian cancer via the miR-17-5p/PIK3R1 ceRNA regulatory axis

LncRNA MNX1-AS1 drives the progression of non-small cell lung cancer and serves as a ceRNA to target COMMD8 by sponging miR-218-5p

The role and mechanistic action of MNX1-AS1 in non-small cell lung cancer (NSCLC) remain unclear. This study aimed to investigate the function of MNX1-AS1 in the progression of NSCLC. A total of 40 paired tumor and adjacent lung tissue samples from patients with NSCLC were collected to investigate the expression of MNX1-AS1. H1299 and HCC827 cells were transfected with sh-MNX1-AS1, shRNA-NC, miR-218-5p mimic, mimic-NC, pcDNA3.1-COMMD8, or empty vector (pcDNA3.1). The expression of MNX1-AS1, miR-218-5p, and COMMD8 was detected using quantitative real-time PCR (qRT-PCR). Cell proliferation was evaluated using CCK-8 assays, while cell migration and invasion were evaluated using Transwell assays. Dual-luciferase reporter and RNA pull-down assays were performed to validate the targeting interactions between MNX1-AS1 and miR-218-5p, as well as between COMMD8 and miR-218-5p. In vivo, a nude mouse model was established: tumor volume and weight were measured after four weeks. Gene expression in tumor tissue was quantified using qRT-PCR, and Ki-67 expression was evaluated using immunohistochemistry. MNX1-AS1 expression was significantly upregulated in NSCLC tissues (P < 0.05) and was correlated with poor prognosis in NSCLC patients. MNX1-AS1 knockdown markedly suppressed the viability, migration, and invasion of H1299 and HCC827 cells (P < 0.05). Mechanistically, MNX1-AS1 acted as a molecular sponge for miR-218-5p, thereby relieving miR-218-5p-mediated repression of its direct target COMMD8 (P < 0.05). Functional rescue experiments revealed that miR-218-5p silencing or COMMD8 overexpression partially reversed the inhibitory effects of MNX1-AS1 knockdown on the cell viability, migration, and invasion of H1299 and HCC827 cells. In vivo, sh-MNX1-AS1 significantly reduced tumor volume and weight (P < 0.05). Moreover, the expression of MNX1-AS1, COMMD8, and Ki-67 were downregulated, while the expression of miR-218-5p was upregulated in sh-MNX1-AS1 tumor tissues (P < 0.05). MNX1-AS1 promotes the progression of NSCLC by modulating the miR-218-5p/COMMD8 axis.