SNHG12/miR-326/E2F1 feedback loop facilitates the progression of oral squamous cell carcinoma

Abstract

Oral squamous cell carcinoma (OSCC) is a kind of common malignant tumor worldwide. An increasing number of researches have validated that long non-coding RNAs (lncRNAs) are closely associated with the occurrence and development of multiple diseases, including cancers. However, the role of lncRNA SNHG12 in OSCC was largely unknown. In present study, qRT-PCR manifested the upregulation of SNHG12 expression in OSCC tissues and cells. Suppression of SNHG12 inhibited cell proliferation, migration, invasion, and EMT process in OSCC. Additionally, SNHG12 depletion also attenuated OSCC tumor growth in vivo. Thereafter, E2F1 was found to be a transcription factor of SNHG12 to stimulate its expression. More interestingly, SNHG12 deficiency reduced E2F1 expression in turn. MiR-326 was found to be shared between SNHG12 and E2F1. Besides, SNHG12 augmented E2F1 in OSCC through miR-326 sequestration. Finally, rescue assays demonstrated that overexpressed E2F1 restored the inhibitory effect resulted from SNHG12 silence, indicating that SNHG12 promoted the progression of OSCC by E2F1-dependent way. This research unveiled that SNHG12/miR-326/E2F1 feedback loop facilitated OSCC progression, which shed new light on therapeutic methods in OSCC.