Table 1. Preclinical studies supporting autophagy inhibition for cancer treatment Cancer type Treatment Breast cancer γ ‐radiation Accelerated cell death by autophagy inhibition Early step Late step siRNA Reference Bcelin 1, ATG3, ATG4b, Apel et al., 2008 ATG4c, ATG5, ATG12 Colorectal cancer Glioma Multiple myeloma (MM) Prostate cancer Skin cancer Lymphoma Gastrointestinal stromal tumors (GISTs) Gastric cancer Chronic myeloid leukemia (CML) SAHA OSI‐027 (mTOR) Tamoxifen Bortezomib Trastuzumab Sulforaphane Bortezomib γ ‐radiation 5‐FU Sulforaphane Temozolomide 4‐HPR γ ‐radiation Imatinib PI‐103 Rapamycin Imatinib Imatinib Bortezomib Androgen deprivation ADI‐PEG20 (arginine deiminase) Saracatinib (Src kinase) Cisplatin Tamoxifen Imatinib Quercetin of rapidly dividing tumor cells) induces autophagy as the cells seek an alternative source of energy and metabolites (Onodera and Oshumi, 2005; Degenhardt et al., 2006; Jones and Thompson, 2009; Rosenfeldt and Ryan, 2009; Rabinowitz and White, 2010). Furthermore, autophagy may also be induced as an adaptive cellular response to various cancer therapies, leading to chemoresistance and cancer cell survival (Chen and Karantza- Wadsworth, 2009; White and DiPaola, 2009). A number of studies in various cancers have examined the inhibition of autophagy through pharmacological means, such 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA 3‐MA BFA BFA BFA BFA BFA BFA CQ CQ CQ CQ CQ CQ BFA, RTA 203 BFA, Monensin CQ, BFA BFA ATG5, Beclin 1, ATG7 LC3, HDAC6, ATF4 LC3 Beclin 1 Beclin 1, ATG5, ATG7, UVRAG ATG7 Beclin 1, ATG5 ATG5, ATG7 Beclin1 Beclin1 ATG7 ATG5 shATG5 Autophagy and cancer 111 Schoenlein et al., 2009 Milani et al., 2009 Vazquez‐Martin et al., 2009 Kanematsu et al., 2010 Fels et al., 2008 Apel et al., 2008 Li et al., 2010 Nishikawa et al., 2010 Kanzawa et al., 2004 Tiwari et al., 2008 Lomonaco et al., 2009 Shingu et al., 2009 Fan et al., 2010 Fan et al., 2010 Carew et al., 2007 Yogalingam and Pendergast, 2008 Bellodi et al., 2009 Crowley et al., 2011 Kawaguchi et al., 2011 Li et al., 2008 Kim et al., 2009 Wu et al., 2010 Claerhout et al., 2010 Amaravadi et al., 2007 Gupta et al., 2010 CQ, Quinacrine ATG7, ATG12 ATG5, Beclin1 Wang et al., 2011 as treatment with 3-methyladenine (3-MA, a PI3K III inhibitor), bafilomycin A (a specific inhibitor of vacuolar-type H+-ATPase), chloroquine (CQ) or hydroxychloroquine (HCQ) (lysosomotropic agents that impair fusion between autophagosomes and lysosomes), or by knockdown of autophagy- related genes, such as ATG5, ATG6 and ATG7. Table 1 summarizes preclinical studies supporting autophagy inhibition as an anticancer strategy. Notably, these inhibitions sensitized cancer cells to a wide range of therapeutic modalities, including genotoxic chemo- and radio-therapy, hormonal