Background Chemotherapy in conjunction with surgical operations have been commonly used for the treatment of many tumors. However, a significant number of tumors fail respond to radiation therapy and/or chemotherapy because many forms of tumors appear to become less sensitive or resistant to radiation and anticancer drugs after consecutive treatments. Although extensive studies on the molecular mechanisms of resistance to chemo- and/or radiation therapy have been carried out, problems related to overcoming this resistance remain to be solved. Romo1 is a nuclear-encoded small transmembrane protein located in mitochondrial inner membrane. It is known to induce mitochondrial reactive oxygen species (ROS) production in response to various cellular stresses. For a decade, Romo1 has been studied in the context of mitochondrial ROS production, cancer cell invasion, inflammation, replicative senescence, and mitochondrial dynamics.
Materials and Methods We identified a Romo1 antagonist and tried to its efficacy as chemotherapy sensitizer using cancer cells and animal models.
Results A Romo1 antagonist can enhance the cellular levels of ROS, leading to tumor cell death. Its treatment induced the elevation of chemotherapy-induced oxidative damage of cancer cells. We also treated the Romo1 antagonist in combination with various chemotherapeutic agents.
Conclusions We suggest that Romo1 antagonist can enhance the cellular levels of ROS, leading to elevation of chemotherapy-induced oxidative damage of cancer cells. We also suggest that Romo1 is the new target to identify effective substances for development of chemotherapy sensitizer.
Disclosure Information Y. Yoo: None. D. You: None. J. Park: None. H. Kim: None.
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