Long noncoding RNA SNHG22 increases ZEB1 expression via competitive binding with microRNA-429 to promote the malignant development of papillary thyroid cancer.

摘要: Long noncoding RNA termed small nucleolar host gene 22 (SNHG22) is a crucial regulator in epithelial ovarian carcinoma. Nevertheless, the regulatory functions of SNHG22 papillary thyroid cancer (PTC) progression and its mechanisms action remain poorly defined. Therefore, present study aimed to investigate role malignant phenotype PTC determine whether regulates via ceRNA mechanism. expression was detected using reverse transcription-quantitative polymerase chain reaction analysis. The biological actions silencing cells were evaluated both vitro (using Cell Counting Kit-8 assay, flow cytometry analysis, cell migration invasion assays) vivo tumorigenicity assay). Herein, high observed tissues lines. This level closely associated with unfavorable clinicopathological characteristics worse overall survival patients PTC. knockdown effectively suppressed proliferation, migration, vitro; accelerated apoptosis; hindered tumor growth vivo. Mechanistic experiments revealed that directly interacts microRNA-429 (miR-429) as an miRNA sponge positively modulates ZEB1 expression. Rescue assays found miR-429 inhibition or upregulation can offset cells. In sum, SNHG22, miR-429, form interactive network cancer-promoting roles cells, suggesting SNHG22/miR-429/ZEB1 pathway novel diagnostic therapeutic target.