Bladder cancer (BCa) is the fourth most common urological malignancy in the world, it has become the costliest cancer to manage due to its high rate of recurrence and lack of effective treatment modalities. As a natural byproduct of cellular metabolism, reactive oxygen species (ROS) have an important role in cell signaling and homeostasis. Although up-regulation of ROS is known to induce tumorigenesis, growing evidence suggests a number of agents that can selectively kill cancer cells through ROS induction. In particular, accumulation of ROS results in oxidative stress-induced apoptosis in cancer cells. So, ROS is a double-edged sword. A modest level of ROS is required for cancer cells to survive, whereas excessive levels kill them. This review summarizes the up-to-date findings of oxidative stress-regulated signaling pathways and transcription factors involved in the etiology and progression of BCa and explores the possible therapeutic implications of ROS regulators as therapeutic agents for BCa.
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