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Fig. 6 | Cancer Communications

Fig. 6

From: Aldolase A promotes proliferation and G1/S transition via the EGFR/MAPK pathway in non-small cell lung cancer

Fig. 6

Mutual regulation relationship between ALDOA and epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) pathway. a Key components of the EGFR/MAPK pathway were measured by western blotting. β-actin was used as loading control. The results showed that EGFR, p-EGFR (Tyr1068), Raf-1, p-Raf-1 (Ser259) and p-MEK1/2 (Ser217/S221) were decreased and that p-ERK1/2 (Thr202/Tyr204) was upregulated in shAL cells compared with shNC cells. b Immunofluorescence assays of EGFR and p-EGFR (Tyr1068). EGFR or p-EGFR (Tyr1068) was labeled with fluorescein isothiocyanate-conjugated antibody (green), and the nucleus was labeled by 4′,6-diamidino-2-phenylindole (blue). ALDOA-knockdown H520 cells exhibited weaker staining of EGFR and p-EGFR (Tyr1068) compared with negative control cells. c ALDOA distribution after MEK1/2 inhibition. Nuclear and cytoplasmic proteins of H520 cells were separately extracted after U0126-EtOH treatment. The ALDOA and p-ERK1/2 distributions were examined by western blotting. Octamer-binding transcription factor-1 (Oct-1) or β-tublin was used as a loading control of the nucleus or the cytoplasm

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