Figure 7
A correlation between LC3B mRNA level and sensitivity of Sal in melanoma. (a) The mRNA levels of LC3B were analyzed using real-time PCR assay, and normalized with the amount of B2M mRNA. (b) Linear regression analysis was performed to identify the potential correlation between LC3B expression and inhibition rate of Sal treatment (1 μM, 7 days) on clinical melanoma samples. (c) Model of the action of Sal in SK-Mel-19 cells. Sal which disrupted the balance of Na+ and K+ triggered ER stress and a decrease of mitochondrial ΔΨ, thus leading to UPR and damaged mitochondria. To keep its stability balance and normal function, cells produced autophagosomes to degrade those damaged organelles. However, Sal not only induced autophagy, but also inhibited the fusion between autophagosomes and lysosomes, causing an aberrant autophagic flux. Finally, accumulations of autophagosomes lead to autophagic cell death.
