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

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 SNH...

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Published inOral diseases Vol. 26; no. 8; pp. 1631 - 1639
Main Authors Yin, Yue, Tan, Yingyun, Yao, Yuan, Lu, Na, Zhang, Fugui
Format Journal Article
LanguageEnglish
Published Denmark Wiley Subscription Services, Inc 01.11.2020
Subjects
Apoptosis
Carcinoma, Squamous Cell - genetics
Cell Line, Tumor
Cell migration
Cell proliferation
E2F1
E2F1 Transcription Factor - genetics
Feedback
Head and Neck Neoplasms
Humans
MicroRNAs - genetics
miR‐326
Mouth Neoplasms - genetics
Non-coding RNA
Oral cancer
Oral squamous cell carcinoma
RNA, Long Noncoding - genetics
SNHG12
Squamous cell carcinoma
Squamous Cell Carcinoma of Head and Neck
E2F1
oral squamous cell carcinoma
SNHG12
miR-326
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Summary: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.
Bibliography:Yue Yin and Yingyun Tan are cofirst authors.
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ISSN:1354-523X
1601-0825
DOI:10.1111/odi.13458