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

Nanoscale Research Letters

Yan Zhang¹  Fei Na¹  Wei Zhao¹  Meng Li¹  Shengchun Tong¹ 

[1] Department of Gynecology, The Fourth Affiliated Hospital of China Medical University, No. 4, Chongshan East Road, Huanggu District, 110032, Shenyang, China;

关键词: Endometrial cancer;    LINC01354;    MicroRNA-216b;    Kirsten rat sarcoma viral oncogene;    Tumorigenesis;   

DOI  :  10.1186/s11671-021-03640-w

来源: Springer

【 摘 要 】

ObjectiveLINC01354 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.MethodsMeasurements 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.ResultsIncreased 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.ConclusionIt is testified that silencing LINC01354 inhibits KRAS by up-regulating miR-216b, thereby discouraging cell malignant phenotype in EC.

【 授权许可】

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