Background: Long non-coding RNA LINC00511 is known to exacerbate lung adenocarcinoma (LUAD) progression. However, the specific mechanism by which LINC00511 affects LUAD progression has not been investigated as yet, and we aimed to elucidate the same in the present study.
Methods: The expression levels of LINC00511, microRNA miR-4739, and pyrroline-5-carboxylate reductase 1 (PYCR1) were determined by quantitative reverse transcription PCR and Western blotting. The Cell Counting Kit-8 and bromodeoxyuridine assays were used to evaluate cell proliferation. Apoptosis was evaluated by flow cytometry, and Bax and Bcl-2 protein levels were determined by western blotting. Cell migration was assessed using transwell assay. The interaction between LINC00511, miR-4739, and PYCR1 was analyzed using luciferase, RNA immunoprecipitation, and RNA pull-down assays.
Results: The expression levels of LINC00511 and PYCR1 in LUAD were downregulated, whereas that of miR-4739 was upregulated. Functional studies showed that knockdown of LINC00511 or PYCR1 suppressed the proliferation and migration of LUAD cells, and promoted apoptosis. On the contrary, knockdown of miR-4739 had tumor-promoting effects. Mechanistically, LINC00511 prevented the miR-4739 led inhibition of PYCR1, resulting in PYCR1 overexpression.
Conclusion: This study demonstrates for the first time that LINC00511 aggravates the malignancy of LUAD by sponging miR-4739 to upregulate PYCR1 expression.
Keywords: LINC00511; PYCR1; apoptosis; lung adenocarcinoma; miR-4739.
© 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.