LINC01117 promotes the malignant proliferation of lung adenocarcinoma by increasing HOXD8 mRNA stability

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The present study aimed to investigate the functional role and molecular mechanisms of long intergenic non‑protein coding RNA 1117 (LINC01117) in lung adenocarcinoma (LUAD). Bioinformatics analysis was performed to assess the expression level and prognostic value of LINC01117. Gene expression in LUAD and lung squamous cell carcinoma tissues was determined by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), and gene and protein expression levels in LUAD cells were detected using RT‑qPCR and western blotting, respectively. Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine, live cell imaging and colony formation assays were used to evaluate the proliferation of LUAD cells. Actinomycin D was used to inhibit RNA transcription. The results indicated that LINC01117 was significantly upregulated in both LUAD and lung squamous cell carcinoma, and its elevated expression was positively associated with poor prognosis in LUAD. Knockdown of LINC01117 inhibited cell proliferation, whereas its overexpression promoted proliferation. Furthermore, LINC01117 exhibited positive co‑expression with the transcription factor homeobox D8 (HOXD8); knockdown or overexpression of LINC01117 reduced or increased HOXD8 expression at both the RNA and protein levels, respectively. Conversely, HOXD8 knockdown did not significantly alter LINC01117 expression; however, HOXD8 knockdown inhibited cell proliferation and reversed the pro‑proliferative effects induced by LINC01117 overexpression. Mechanistically, LINC01117 was associated with increased HOXD8 mRNA stability. In conclusion, LINC01117 may serve as a notable prognostic biomarker that promotes cell proliferation in LUAD. HOXD8 may function as a downstream target of LINC01117, with LINC01117 exerting its pro‑proliferative effects by increasing HOXD8 mRNA stability.

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