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. 2021 Sep 20;40:294. doi: 10.1186/s13046-021-02096-1

Fig. 8.

Fig. 8

FTO/LINC00022 axis drives ESCC tumorigenesis. (A) Deletion of LINC00022 attenuated the proliferative effects induced by FTO over-expression in KYSE70 cells, *p < 0.05. (B) Ectopic expression of FTO partially relieved the inhibitory effects of proliferation caused by LINC00022 ablation in KYSE150 cells, *p < 0.05; **p < 0.01. (C) The non-population-dependent growth ability of ESCC cells under the control of the FTO/LINC00022 axis was evaluated by the colony formation assay, *p < 0.05. (D-E) PI-labeling staining combined with flow cytometry indicated the role of FTO/LINC00022 axis in ESCC cell-cycle progression, *p < 0.05; **p < 0.01. (F-G) Western blot was used to investigate the changes of cell cycle regulator protein levels, p16, p21 and p53 in KYSE70 (F) and KYSE150 (G) cells following FTO-LINC00022 cross-talking. (H) Knockdown of LINC00022 fully rescued the growth promotion effect induced by ectopic FTO expression on KYSE70 cells in nude mice (n = 3) (left panel). The tumor volume was measured every three days from day 9 to day 21 after cell inoculation, and the curve was plotted (right panel), *p < 0.05. (I) Over-expression of FTO partially attenuated the inhibition of subcutaneous tumorigenicity caused by LINC00022 knockdown on KYSE150 cells in nude mice (n = 4) (left panel). The tumor volume was monitored every five days from day 10 to day 30 after cell inoculation, and the curve was generated (right panel), *p < 0.05