Also, SLC1A5 overexpression abolished the inhibition effect of miR-1827 on NSCLC cell progression. The rescue experiments showed that miR-1827 inhibitor reversed the suppressive effect of circ_0000808 knockdown on the malignant behaviors of NSCLC cells. Further results confirmed that circ_0000808 interacted with miR-1827 to positively regulate SLC1A5. ResultsĬirc_0000808 expression was upregulated in NSCLC tissues and cancer cells, and its silencing inhibited NSCLC cell proliferation, migration, and invasion and led to apoptosis. Xenograft mouse model was used to assess the in vivo effects of circ_0000808.
Cell glutamine metabolism was assessed by determining glutamine uptake, glutamate production, and α-ketoglutarate production. Dual-luciferase reporter assay and RIP assay were used to investigate the interactions between miR-1827 and circ_0000808 or SLC1A5. The protein expression was measured by Western blot analysis. Cell proliferation, apoptosis, migration, and invasion were measured by cell counting kit 8 assay, colony formation assay, EdU staining, flow cytometry, wound healing assay, and transwell assay. Quantitative real-time PCR was used to detect the expression of circ_0000808, miR-1827, and solute carrier family 1 member 5 (SLC1A5).
However, the function and molecular mechanism of circ_0000808 in non-small cell lung cancer (NSCLC) are still unclear. Circular RNA (circRNA) has been proved to be an important molecular target for cancer treatment.
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