Autophagy regulation in bladder cancer as the novel therapeutic strategy

Ji-Fan Lin, Thomas I. S. Hwang


Being the most common tumor of the urinary tract, bladder cancer (BC) has a prolonged nature that like many chronic disease requiring careful and invasive long-term surveillance. Among cancers, BC has the highest costs per patient making it an economic burden in medical treatment. The 2016 Nobel Prize in Physiology or Medicine was awarded to the researcher that revealed the mechanism of autophagy. Autophagy is an evolutionally conserved catabolic process that cells degrade cytoplasmic organelles or constituents through lysosome to generate energy and maintain homeostasis for cellular survival and proliferation. Autophagy is now recognized to play important role in both normal tissue and tumor development. In cancer cells, autophagy is usually constitutively activated due to the deregulation of PI3K/ Akt/mTOR pathway that enables them to adapt efficiently to an unfavorable hypo-nutrient conditions in the tumor microenvironment. Therefore, targeting autophagy to reduce tumor growth or attenuate treatment resistance has led to greater interest in the field of cancer research, including the role of autophagy in BC. In this review, we summarize the studies from others and our own group regarding the role of autophagy in BC progression and treatment resistant by systematically reviewing treatment modalities including intravesical installation and chemotherapy for non-muscle invasive bladder cancer (NMIBC) and muscle invasive bladder cancer (MIBC).