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Existing knowledge regarding the involvement of lncRNA OIP5-AS1 in lung adenocarcinoma (LUAD) development is still incomplete and requires further investigation. Our research aimed to reveal the function of OIP5-AS1 in LUAD. We evaluated the level of OIP5-AS1 and its association with clinicopathological factors in LUAD. The research examined the potential implications of targeting OIP5-AS1 in mitigating the invasive properties of lung cancer cells. A nude mouse xenograft model was utilised to examine tumour growth. We used bioinformatics data and a dual-luciferase reporter assay to study the interactions between OIP5-AS1 and hsa-miR-29b-3p. OIP5-AS1 was significantly overexpressed in LUAD, with a higher level correlating with adverse clinicopathological features. Knockdown of OIP5-AS1 resulted in notable decreases in LUAD cell growth, movement, and aggressive behaviour, accompanied by a decrease in tumour size in vivo. Furthermore, OIP5-AS1 was confirmed to act as a molecular sponge for hsa-miR-29b-3p. The elevated expression of hsa-miR-29b-3p intensified the inhibitory outcomes of OIP5-AS1 knockdown on LUAD cell properties. ZIC5 was experimentally determined to be a direct molecular target of hs-miR-29b-3p, emphasising its integral position in the regulatory interaction. This study reveals a new regulatory route involving OIP5-AS1, hsa-miR-29b-3p and ZIC5 in LUAD pathogenesis. Given its oncogenic traits, OIP5-AS1 presents a promising predictive biomarker and therapeutic target for optimising lung cancer treatment.
Liang et al. (Thu,) studied this question.
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