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Abstract
Long non-coding RNAs (lncRNAs) have been confirmed as crucial regulators in tumorgenesis.
Small nucleolar RNA host gene 16 (SNHG16) has been recently uncovered to be a potential
oncogene in several types of cancers. However, its expression level and potential
role in cervical cancer remain uncertain. In our research, we assessed the expression
level of SNHG16 in clinical cervical cancer tissues and cells. We made use of functional
assays to determine the biological effects of SNHG16 on cell proliferation and migration
of cervical cancer. By employing the bioinformatics analysis tools, we revealed that
miR-216-5p could interact with SNHG16 and there existed a negative correlation between
the expression levels of miR-216-5p and SNHG16 in cervical cancer specimens. Furthermore,
RIP assay, RNA pulldown system and dual luciferase reporter assays confirmed that
SNHG16 directly targeted miR-216-5p by harboring the binding sites of microRNA in
the SNHG16 sequence. Additionally, bioinformatics analysis provided an evidence that
ZEB1 was a potential target of miR-216-5p. Collectively, it was suggested that SNHG16
could serve as an oncogene that promoted tumor progression by acting as an endogenous
'sponge' to regulate miR-216A-5p/ZEB1.