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Background  Emerging studies have shown that long noncoding RNAs (lncRNAs) predominantly function in the carcinogenesis of multiple developing human tumors. The current study aimed to investigate the underlying mechanisms of  LINC00337  in lung adenocarcinoma.    Methods  We analyzed TCGA and GTEx datasets and chose  LINC00337  as the research object. Cell proliferation, cell apoptosis, cell cycle, migration, and invasion were detected in the gain and loss experiments of  LINC00337  both in vitro and in vivo. Moreover, RNA pull-down, luciferase reporter assays, western blotting analysis, and rescue experiments were performed to investigate the underlying molecular mechanisms of  LINC00337  function.    Results   LINC00337  expression was remarkably upregulated in lung adenocarcinoma. In addition,  LINC00337  knockdown was shown to repress cell migration, invasion, and proliferation, as well as the cell cycle, and gear up apoptosis in lung adenocarcinoma in vitro and in vivo. With respect to the mechanism,  LINC00337  knockdown boosted miR-1285-3p expression and then restrained  YTHDF1  expression post-transcriptionally. Crucially, both miR-1285-3p decrement and  YTHDF1  overexpression successfully reversed the influence on cell proliferation, migration, invasion, and apoptosis caused by  LINC00337  shRNA.    Conclusions  These results suggest that  LINC00337  acts as an oncogenic lncRNA, targeting miR-1285-3p and regulating  YTHDF1  expression, to promote the progression of lung adenocarcinoma.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12935-021-02253-8.

LncRNA LINC00337 sponges mir-1285-3p to promote proliferation and metastasis of lung adenocarcinoma cells by upregulating YTHDF1