LncRNA SNHG17 regulates cell proliferation and invasion by targeting miR-338-3p/SOX4 axis in esophageal squamous cell carcinoma

• Published in: Cell death & disease 2021-08, Vol.12 (9), p.806-806, Article 806
• Main Authors: Chen, Wenhu, Wang, Lifang, Li, Xiaoyan, Zhao, Changan, Shi, Liang, Zhao, Hongguang, Huang, Chen
• Format: Article
• Language: English
• Subjects: 13/51; 14/32; 14/34; 42/109; 42/89; 45/61; 45/90; 631/337/384; 692/420/755; 692/699/67/1504/1477; 82/1; Animals; Antibodies; Base Sequence; Biochemistry; Biomedical and Life Sciences; Cell Biology; Cell Culture; Cell growth; Cell Line, Tumor; Cell proliferation; Cell Proliferation - genetics; Esophageal cancer; Esophageal Neoplasms - genetics; Esophageal Neoplasms - pathology; Esophageal Squamous Cell Carcinoma - genetics; Esophageal Squamous Cell Carcinoma - pathology; Esophagus; Female; Gene Expression Regulation, Neoplastic; Genes, Tumor Suppressor; Humans; Immunology; Life Sciences; Male; Mesenchyme; Mice; Mice, Inbred BALB C; Mice, Nude; MicroRNAs - genetics; MicroRNAs - metabolism; Middle Aged; Neoplasm Invasiveness; Nucleoli; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; snoRNA; SOXC Transcription Factors - genetics; SOXC Transcription Factors - metabolism; Squamous cell carcinoma; Tumorigenesis; Tumors; Up-Regulation - genetics
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-021-04093-w

Small nucleolar RNA host gene 17 (SNHG17), a novel functional long noncoding RNA, has been demonstrated to play an essential role in the oncogenesis of several tumors. However, for esophageal squamous cell carcinoma (ESCC) the expression pattern and detailed function of SNHG17 are largely unknown. Hence, we conducted this study to explore potential roles and underlying oncogenic mechanisms for SNHG17 in ESCC progression. Results demonstrated SNHG17 to be markedly upregulated in ESCC. Knockdown of SNHG17 significantly suppressed ESCC cell proliferation, invasion, and epithelial–mesenchymal transition in vitro and tumor growth in vivo. Online database software analysis found miR-338-3p to interact with SNHG17 with the level of miR-338-3p negatively correlated with SNHG17 levels in ESCC samples. Further, miR-338-3p was found to directly target SRY-box transcription factor 4 (SOX4) in ESCC cells. Mechanistic analysis suggested that SNHG17 acts as an endogenous “sponge” competing with miR-338-3p to regulate SOX4, thereby promoting tumor progression. These results suggest that these molecular interactions may be potential therapeutic targets for ESCC.