biostudies-literatureLambring CBNIMHD NIH HHSNational Institutes of HealthNIGMS NIH HHSCancer Prevention and Research Institute of Texas207-216https://www.ebi.ac.uk/biostudies/studies/S-EPMC11192519biostudies-literatureUnknown137Therapeutic targeting of Sp1 transcription factor and survivin, are studied in various cancers due to their consistent overexpression. These markers result in poorer cancer prognoses and their downregulation has been investigated as an effective treatment approach. Mithramycin-A and Tolfenamic acid are two drugs with innate anti-cancer properties and are suggested to be able to target Sp1 through GC/GT DNA binding interference, however in-depth binding and mechanistic studies are lacking. Through docking analysis, we investigated Mithramycin-A and Tolfenamic acid in terms of their specific binding interactions with Sp1 and survivin. Through further molecular dynamics simulations including Root Mean Square (RMS) Fluctuation and RMS Deviation, rGYr, and H-bond analysis, we identified criticaProcess biochemistry (Barking, London, England)Docking and molecular dynamic simulations of Mithramycin-A and Tolfenamic acid against Sp1 and survivin.PMC11192519RP2100462U54MD006882–06S21 MD012472U54 MD0068821S21MD012472–01R25 GM125587Lambring CBBehera SKBasha RFiadjoe HfalseDocking and molecular dynamic simulations of Mithramycin-A and Tolfenamic acid against Sp1 and survivin.Therapeutic targeting of Sp1 transcription factor and survivin, are studied in various cancers due to their consistent overexpression. These markers result in poorer cancer prognoses and their downregulation has been investigated as an effective treatment approach. Mithramycin-A and Tolfenamic acid are two drugs with innate anti-cancer properties and are suggested to be able to target Sp1 through GC/GT DNA binding interference, however in-depth binding and mechanistic studies are lacking. Through docking analysis, we investigated Mithramycin-A and Tolfenamic acid in terms of their specific binding interactions with Sp1 and survivin. Through further molecular dynamics simulations including Root Mean Square (RMS) Fluctuation and RMS Deviation, rGYr, and H-bond analysis, we identified critica2024-01-01T00:00:00Z2024 Feb2026-06-01T18:12:51.254Z2025-04-05T19:18:54.662ZS-EPMC111925193891241310.1016/j.procbio.2023.12.014