LncRNA SNHG17 regulates cell proliferation and invasion by targeting miR-338-3p/SOX4 axis in esophageal squamous cell carcinoma
Autor: | Xiaoyan Li, Changan Zhao, Wenhu Chen, Chen Huang, Lifang Wang, Hongguang Zhao, Liang Shi |
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Rok vydání: | 2021 |
Předmět: |
Male
Cancer Research Esophageal Neoplasms Immunology Mice Nude Biology medicine.disease_cause Article Non-coding RNAs SOXC Transcription Factors Cellular and Molecular Neuroscience SOX4 Downregulation and upregulation Cell Line Tumor medicine Animals Humans Genes Tumor Suppressor Neoplasm Invasiveness RNA Messenger Transcription factor neoplasms Oncogenesis Cell Proliferation Gene knockdown Mice Inbred BALB C QH573-671 Base Sequence Cell growth Oesophageal cancer Cell Biology Middle Aged Long non-coding RNA digestive system diseases Up-Regulation Gene Expression Regulation Neoplastic MicroRNAs Tumor progression Cancer research Female RNA Long Noncoding Esophageal Squamous Cell Carcinoma Carcinogenesis Cytology |
Zdroj: | Cell Death & Disease Cell Death and Disease, Vol 12, Iss 9, Pp 1-10 (2021) |
ISSN: | 2041-4889 |
Popis: | 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. |
Databáze: | OpenAIRE |
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