We have shown that RMS cells are not able to overexpress ANKRD1 protein, which can be attributed to its proteasomal degradation. The unsuccessful attempt to overexpress ANKRD1 in RMS cells indicates the possibility that its overexpression may have detrimental effects for RMS cells and opens a window for further research into its role in RMS pathogenesis and for potential therapeutic targeting.
Proteasomal degradation was inhibited by the incubation of cells with MG132...ANKRD1 propensity for proteasomal degradation indicates that ANKRD1 overexpression may be lethal for RMS cells. These observations suggest that ANKRD1 warrants further consideration as RMS therapeutic target.