J Cancer 2020; 11(3):759-768. doi:10.7150/jca.33267 This issue
1. Stomatological Hospital of Chongqing Medical University, Chongqing, China.
2. Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China.
3. Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China.
An increasing number of studies indicate that miR-144-3p is dysregulated in numerous cancers, but its role in oral squamous cell carcinoma (OSCC) remains largely unknown. Herein we demonstrated that miR-144-3p expression was significantly downregulated in OSCC tissues and cell lines. Moreover, the low level of miR-144-3p expression was associated with the clinical characteristics of OSCC patients. Furthermore, ectopic expression of miR-144-3p inhibited the proliferation, migration, and invasion of OSCC cells in vitro, and blunted the tumorigenic ability of OSCC cells in vivo. Additionally, the levels of miR-144-3p were negatively correlated with the expression status of endoplasmic reticulum oxidoreduction-1-like (ERO1L) in OSCC cell lines. Subsequently, we identified that ERO1L was a direct target of miR-144-3p. Intriguingly, we found that miR-144-3p downregulation of ERO1L inhibited the activity of signal transducer and activator of transcription 3 (STAT3) in OSCC cells. Therefore, miR-144-3p suppresses tumorigenesis by targeting ERO1L/STAT3 signaling pathway in OSCC. miR-144-3p may a candidate target for OSCC treatment.
Keywords: miR-144-3p, ERO1L, STAT3, tumorigenesis, OSCC