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

AbstractOBJECTIVE:
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.
AuthorsYan Zhang, Wei Zhao, Fei Na, Meng Li, Shengchun Tong
JournalNanoscale research letters (Nanoscale Res Lett) Vol. 17 Issue 1 Pg. 21 (Jan 31 2022) ISSN: 1931-7573 [Print] United States
PMID35099637 (Publication Type: Journal Article, Retracted Publication)
Copyright© 2021. The Author(s).

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