Cyclin C: A new responser for chemosensitivity in cancer

The resistance to cisplatin-based chemotherapy is a common cause of poor prognosis in cancer patients. Cisplatin stimulation causes cyclin C translocating to mitochondria, and in turn induces mitochondrial fission. However, little is known about the role of cyclin C in mitochondrial dysfunction in cancer cells challenged with cisplatin. In the present commentary, we bring to the attention of readers the recent report by Jiang et al which revealed the importance of ubiquitylation and translocation of cyclin C in gastric cancer cells in response to cisplatin stimulation for mitochondrial stability. This finding provides new insights into exploring the novel mechanisms of chemoresistance and developing the new chemotherapy synergistic agents in the era of precision oncology.

Automated summary

The resistance to cisplatin-based chemotherapy is a common cause of poor prognosis in cancer patients. Recent research has found that ubiquitylation and translocation of cyclin C in cancer cells can affect the stability of mitochondria after cisplatin stimulation, providing new insights for studying chemoresistance mechanisms and developing new chemotherapy drugs.