Objective: To investigate the expression levels of LINC00342 in gastric cancer (GC) tissues and cells and the pathways mediating its effects on biological behaviors of GC cells.
Methods: Bioinformatic analysis was performed to identify the lncRNAs and their downstream miRNAs involved in regulation of biological behaviors of GC cells. qRT-PCR was used to analyze the differential expression of LINC00342 and miR-596 in GC cell lines, human gastric mucosal cells, and GC and adjacent tissues. In human GC MGC-803 and MGC-823 cells, the effects of LINC00342 overexpression, miR-596 overexpression, LINC00342 knockdown, or miR-596 knockdown on cell proliferation, migration, invasion and cell cycle changes were examined using Edu assay, CCK-8 assay, wound healing assay, Transwell assay, and flow cytometry. The regulatory interaction between LINC00342 and miR-596 was investigated using a dual-luciferase reporter assay.
Results: Informatic analysis identified LINC00342 as the candidate lncRNA regulating biological behaviors of GC cells, with miR-596 as its downstream miRNA. LINC00342 expression levels were significantly higher while miR-596 expression levels were lower in GC tissues and cell lines than in the paired adjacent tissues and human gastric mucosal cell lines (all <0.05). In MGC-803 and MGC-823 cells, overexpression of LINC00342 significantly enhanced cell proliferation (<0.05), migration (<0.01), and invasion (<0.001) and reduced the percentage of G0/G1 phase cells (<0.01), while knocking down LINC00342 significantly suppressed cell proliferation (<0.05), migration (<0.01), and invasion (<0.001) and increased G0/G1 phase cell percentage (<0.01). Modulation of miR-596 expression levels produced the opposite effects. Dual-luciferase reporter assay confirmed the specific binding between LINC00342 and miR-596 (=0.0067).
Conclusion: In GC cells, LINC00342 regulates cell proliferation, migration, and invasion by targeting miR-596.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10630212 | PMC |
| http://dx.doi.org/10.12122/j.issn.1673-4254.2023.10.14 | DOI Listing |
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