Inhibition of Autophagy by 3-MA Enhances the Effect of 5-FU-Induced Apoptosis in Colon Cancer Cells

Abstract

Our results suggest that 5-FU-induced apoptosis in colon cancer cells can be enhanced by the inhibitor of autophagy, 3-MA. Autophagy might play a role as a self-defense mechanism in 5-FU-treated colon cancer cells, and its inhibition could be a promising strategy for the adjuvant chemotherapy of colon cancer.

Autophagy protects breast cancer cells from epirubicin-induced apoptosis and facilitates epirubicin-resistance development

“…17,18 A series of studies reported that chemotherapy induced-autophagy promotes the survival of some kinds of cancer cell lines. [19][20][21][22][23] These results suggest that autophagy might be involved in the development of chemotherapy resistance. But few studies on the relationship between autophagy and chemotherapy were reported, especially studies utilizing resistant cancer cells.…”

Autophagy in drug resistance of the multiple myeloma cell line RPMI8226 to doxorubicin

“…Numerous studies have demonstrated that autophagy combats numerous types of adverse stresses and maintains the survival of tumor cells (Li et al, 2009;Carew et al, 2012). Cytotoxic stress and metabolic stress such as hypoxia, nutrition deficiency, chemotherapy, and radiotherapy are common in tumor cells because of their high proliferative activity and high metabolism.…”

Autophagy, senescence and tumor dormancy in cancer therapy

“…5,6 In some studies, autophagy and apoptosis have been found to exert similar levels of toxicity 7,8 while in others a blockade to protective autophagy has resulted in cytotoxicity due to apoptosis. 3,[9][10][11][12] Finally, a recent report presents evidence for apoptosis that is dependent on prior autophagy. The transient arrest and renewed tumor growth that has been interpreted as tumor dormancy by Lu et al 2 is also a common observation in other xenograft models treated with chemotherapy or radiation; 19,20 our own studies in cell culture [21][22][23] also support the concept of drug and radiation induced senescence in tumor cells that is succeeded by proliferative recovery.…”