Autophagy is crucial in the maintenance of homeostasis and regenerated energy of mammalian cells.Macroautophagy and chaperone-mediated autophagy(CMA) are the two best-identified pathways. Recentresearch has found that in normal cells, decline of macroautophagy is appropriately parallel with activationof CMA. However, whether it is also true in cancer cells has been poorly studied. Here we focused on crosstalkand conversion between macroautophagy and CMA in cultured Burkitt lymphoma Raji cells whenfacing serum deprivation and exposure to a toxic compound, arsenic trioxide. The results showed that bothmacroautophagy and CMA were activated sequentially instead of simultaneously in starvation-induced Raji cells,and macroautophagy was quickly activated and peaked during the first hours of nutrition deprivation, and thengradually decreased to near baseline. With nutrient deprivation persisted, CMA progressively increased alongwith the decline of macroautophagy. On the other hand, in arsenic trioxide-treated Raji cells, macroautophagyactivity was also significantly increased, but CMA activity was not rapidly enhanced until macroautophagy wasinhibited by 3-methyladenine, an inhibitor. Together, we conclude that cancer cells exhibit differential responsesto diverse stressor-induced damage by autophagy. The sequential switch of the first-aider macroautophagyto the homeostasis-stabilizer CMA, whether active or passive, might be conducive to the adaption of cancercells to miscellaneous intracellular or extracellular stressors. These findings must be helpful to understand thecharacteristics, compensatory mechanisms and answer modes of different autophagic pathways in cancer cells,which might be very important and promising to the development of potential targeting interventions for cancertherapies via regulation of autophagic pathways.