XIST lost induces ovarian cancer stem cells to acquire taxol resistance via a KMT2C-dependent way.

ABSTRACT:

Background/aims

The expression levels of long non-coding RNA XIST are significantly associated with paclitaxel (Pac) sensitivity in ovarian cancer, but the mechanism of action remains unclear. Therefore, this experimental design was based on lncRNA XIST analysis to regulate the effect of XIST on the tumor stem cell and paclitaxel sensitivity in ovarian cancer.

Methods

Sphere assay and fluorescence activated cell sorting (FACS) were used to determine the expression levels of XIST and sensitivity to paclitaxel treatment. The effect of the proliferation was detected by MTT assay. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for lncRNA XIS and KMT2C. The expression of KMT2C was detected by RT-qPCR and Western blot

SUBMITTER: Huang R 

PROVIDER: S-EPMC7487955 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature