(1) Background: deficiency remains a major adverse event in Multiple Myeloma (MM) despite therapeutic progresses. As it is not possible to target deficiency with pharmacological agents, we explored the possibility of activating another p53 family member, p73, which has not been well studied in myeloma. (2) Methods: Using human myeloma cell lines (HMCLs) with normal or abnormal status, we assessed methylation and expression. (3) Results: Using microarray data, we reported that is weakly expressed in 47 HMCLs and mostly in wild type () HMCLs ( = 0.0029). Q-RT-PCR assays showed that was expressed in 57% of HMCLs (4 out of 7) and 11% of abnormal () HMCLs (2 out of 18) ( = 0.0463). We showed that is silenced by methylation in HMCLs and that decitabine increased its expression, which, however, remained insufficient for significant protein expression. Alkylating drugs increased expression of only in HMCLs but failed to synergize with decitabine in HMCLs. (4) Conclusions: Decitabine and melphalan does not appear as a promising combination for inducing p73 and bypassing p53 deficiency in myeloma cells.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5795990PMC
http://dx.doi.org/10.3390/ijms19010040DOI Listing

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