Lung adenocarcinoma (LUAD), a histological subclass of non‐small‐cell lung cancer, is globally the leading cause of cancer‐related deaths. Long noncoding RNAs (lncRNAs) are emerging as cancer regulators. Zinc finger protein… Click to show full abstract
Lung adenocarcinoma (LUAD), a histological subclass of non‐small‐cell lung cancer, is globally the leading cause of cancer‐related deaths. Long noncoding RNAs (lncRNAs) are emerging as cancer regulators. Zinc finger protein multitype 2 antisense RNA 1 (ZFPM2‐AS1) is an oncogene in gastric cancer, but its functions have not been investigated in LUAD. We showed that ZFPM2‐AS1 expression is high in LUAD samples based on GEPIA database (http://gepia.cancer-pku.cn/) and validated ZFPM2‐AS1 upregulation in LUAD cell lines. Functionally, ZFPM2‐AS1 facilitated proliferation, invasion, and epithelial‐to‐mesenchymal transition of LUAD cells. Thereafter, we found that ZFPM2 was negatively regulated by ZFPM2‐AS1, and identified the suppressive effect of ZFPM2 regulation by ZFPM2‐AS1 on LUAD progression. Mechanistically, we showed that ZFPM2‐AS1 interacted with up‐frameshift 1 (UPF1) to regulate mRNA decay of ZFPM2. Rescue assays in vitro and in vivo confirmed that ZFPM2‐AS1 regulated LUAD progression and tumor growth through ZFPM2. Taken together, our findings demonstrate a role for the ZFPM2‐AS1–UPF1–ZFPM2 axis in LUAD progression, suggesting ZFPM2‐AS1 as a new potential target for LUAD treatment.
               
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