RETRACTED ARTICLE: LINC01354/microRNA-216b/KRAS Axis Promotes the Occurrence and Metastasis of Endometrial Cancer

作者：Yan Zhang, Wei Zhao, Fei Na, Meng Li, Shengchun Tong · 发表于：Nanoscale Research Letters · 年份：2022 · DOI：10.1186/s11671-021-03640-w · 被引用次数：5 · 研究领域：MicroRNA in disease regulation、Circular RNAs in diseases、Cancer-related molecular mechanisms research

OBJECTIVE: LINC01354 has been defined as a tumor driver in several cancers. Nevertheless, whether LINC01354 involves in endometrial cancer (EC) has been little navigated. Thus, the mechanism of LINC01354 was explored in the disease. METHODS: Measurements of LINC01354, microRNA (miR)-216b and kirsten rat sarcoma viral oncogene (KRAS) levels in EC tissues and cells were performed. LINC01354 low expression and miR-216b overexpression vectors were introduced into EC cells (lshikawa), thereby their effects on cell viability, apoptosis, migration and invasion were manifested. Rescue experiments were also carried out by down-regulating LINC01354 and miR-216b spontaneously. Tumorigenesis in vivo was also assessed. The relationships of LINC01354/miR-216b/KRAS were analyzed. RESULTS: Increased LINC01354 and KRAS and reduced miR-216b levels were measured in EC. Silencing LINC01354 or overexpressing miR-216b retarded EC cellular development. LINC01354 counteracted with miR-216b to target KRAS. Suppression of miR-216b antagonized silenced LINC01354-induced impacts on EC cell development. LINC01354/miR-216b/KRAS axis enhanced tumorigenesis in mice with EC. CONCLUSION: It is testified that silencing LINC01354 inhibits KRAS by up-regulating miR-216b, thereby discouraging cell malignant phenotype in EC.