Abstract
We read with great interest the article by Pastukhov et al. (2014a) which reported that NVP-231, the inhibitor of ceramide kinase (CERK), could reduce cell viability, DNA synthesis, colony formation and induced apoptosis of the breast and lung cancer cell lines MCF-7 and NCI-H358. The results suggested that CERK inhibition might be a good potential therapeutic target for breast and lung cancer. Moreover, Pastukhov et al. (2014b) had demonstrated that proliferation was reduced via CERK inhibition in renal mesangial cells and fibroblasts. It suggested that CERK inhibition was a potential target for treating mesangioproliferative kidney diseases. Furthermore, Payne et al. (2014) had indicated that CERK was required for tumour recurrence and survival and CERK was up-regulated in tumour cells and during tumour recurrence in mouse breast cancer. Furthermore, gene expression profiles showed that up-regulated CERK was related to an increased risk of recurrence in women for breast cancer. These results suggested that CERK played a vital role in breast cancer recurrence and CERK inhibition might be a potential target for tumour recurrence. In addition, Bini et al. (2012) had showed that CERK inhibition reduced cell proliferation in human neuroblastoma cells. Together, these findings indicated that CERK played a functional role in diseases. We read with considerable interest and thought that CERK inhibition might be a good potential therapeutic target for diseases, including cancer, mesangioproliferative kidney diseases and neuroblastoma cells.
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