Accumulating evidence shows that elevated levels of reactive oxygen species (ROS) are associated with cancer initiation, growth, and response to therapies. As concentrations increase, ROS influence cancer development in a paradoxical way, either triggering tumorigenesis and supporting the proliferation of cancer cells at moderate levels of ROS or causing cancer cell death at high levels of ROS. Thus, ROS can be considered an attractive target for therapy of cancer and two apparently contradictory but virtually complementary therapeutic strategies for the regulation of ROS to treat cancer. Despite tremendous resources being invested in prevention and treatment for cancer, cancer remains a leading cause of human deaths and brings a heavy burden to humans worldwide. Chemotherapy remains the key treatment for cancer therapy, but it produces harmful side effects. Meanwhile, the process of de novo development of new anticancer drugs generally needs increasing cost, long development cycle, and high risk of failure. The use of ROS‐based repurposed drugs may be one of the promising ways to overcome current cancer treatment challenges. In this review, we briefly introduce the source and regulation of ROS and then focus on the status of repurposed drugs based on ROS regulation for cancer therapy and propose the challenges and direction of ROS‐mediated cancer treatment.

Curcumin is a polyphenolic compound derived from the plant turmeric and the structural instability of which limits its further clinical applications. In this study, 11 curcumin analogs with more stable scaffold were prepared and evaluated. The results indicated that the optimal compound Y-11 exhibited the strongest antiproliferative activities against lung cancer cells including H460 and H1650. Further studies showed that Y-11 potentially inhibited hDHODH, induced cell cycle arrest and apoptosis as well as down-regulated crucial signal pathway protein expression in H1650 cells. In the conclusion, the newly designed curcumin analog Y-11 may be suitable for further development in lung cancer treatment.

Background Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune disease of the central nervous system (CNS) that often causes a range of neuropsychiatric symptoms; but with a relatively low recurrence rate. Anti-NMDAR encephalitis may occur with anti-myelin oligodendrocyte glycoprotein (MOG) encephalitis simultaneously or followed by anti-MOG encephalitis after several months. Case presentation We presented a case of recurrent anti-NMDAR encephalitis followed by anti-MOG encephalitis. A 39-year-old man was admitted to the hospital with five episodes of convulsive seizures, psychoses and memory deficits. With a positive Anti-NMDAR antibody in the cerebrospinal fluid (CSF), after being treated with intravenous immunoglobulins (IVIG) 22.5 g/day for 7 days, intravenous methylprednisolone pulse (IVMP) 500 mg/day for 4 days, and followed by IVMP 250 mg/day for 3 days, the patient was recovered completely. After 1 month, the patient developed disturbances of consciousness, speech difficulties and convulsions. With the positive result of Anti-NMDAR antibodies in the CSF again, we confirmed the diagnosis of recurrent anti-NMDAR encephalitis. The patient was then fully recovered after treatment with IVIG, IVMP and rituximab. Six months later, the patient was readmitted to the hospital with occasional convulsions. With a positive serum MOG antibody and a lesion in the right brainstem by brain magnetic resonance imaging (MRI), the patient was confirmed for anti-MOG encephalitis. The patient was fully recovered again after treatment with IVMP and rituximab, with no neurological sequels remained. Conclusion Patients with positive MOG antibodies are more likely to have brainstem MRI lesions than those with anti-NMDAR encephalitis. Rituximab is recommended for recurrent anti-NMDAR and anti-MOG encephalitis.