Lung squamous cell carcinoma (LUSC) represents one of the commonest types of lung cancer featured with high morbidity and poor prognosis. Many types of research have documented that long noncoding RNAs (lncRNAs) exert crucial functions in the development of cancers, and LUSC is included. In our study, we aimed at unveiling the mechanism underlying long intergenic nonprotein coding RNA 0649 (LINC00649) in LUSC cells. As a result, LINC00649 was discovered to be with high expression in LUSC cells. Moreover, it was confirmed through functional assays that the knockdown of LINC00649 hindered the occurrence and progression of LUSC. Results of mechanism assays validated that E2F transcription factor 7 (E2F7) was a transcription activator of LINC00649 and induced its up-regulation in LUSC cells. Furthermore, LINC00649 recruited TAF15, which is TATA-box binding protein associated factor 15 to stabilize mitogen-activated protein kinase 6 (MAPK6) expression and activate the transcription of MAPK6, thereby enhancing MAPK6 expression to activate the MAPK signaling pathway. Eventually, results of rescue assays suggested that overexpression of MAPK6 offset the influence of LINC00649 silencing on LUSC progression. In summary, our research determined the E2F7/LINC00649/TAF15/MAPK6/MAPK signaling pathway in regulating LUSC development, which made LINC00649 a potential biomarker for LUSC treatment.
© 2022. The Author(s), under exclusive licence to Springer Nature America, Inc.