Here,　we　investigated　the　role　of　one　gene　that　has　been　previously　associated　with　human　prostate　carcinoma　cells-myelodysplasia/myeloid　leukemia　factor　1　interacting　protein　(MLF1IP)-in　order　to　better　ascertain　its　role　in　human　prostate　carcinogenesis.　The　prostate　cancer　cell　line　PC-3　was　lentivirally　transfected　to　silence　endogenous　MLF1IP　gene　expression,　which　was　confirmed　by　real-time　quantitative　PCR　(RT-qPCR).　Cellomics　ArrayScan　VTI　imaging　and　MTT　assays　were　conducted　to　assess　cell　proliferation.　Cell　cycle　phase　arrest　and　apoptosis　were　assayed　by　flow　cytometry.　Colony　formation　was　assessed　by　fluorescence　microscopy.　MLF1IP　gene　expression　was　also　analyzed　by　RT-qPCR　in　sixteen　prostate　cancer　tissue　samples　and　six　healthy　control　prostate　tissue　samples　from　human　patients.　Cell　proliferation　was　significantly　inhibited　in　MLF1IP-silenced　cells　relative　to　control　cells.　G1　phase,　S　and　G2/M　phase　cell　counts　were　not　significantly　changed　in　MLF1IP-silenced　cells　relative　to　control　cells.　Apoptosis　was　significantly　increased　in　MLF1IP-silenced　cells,　while　MLF1IP-silenced　cells　displayed　a　significantly　reduced　number　of　cell　colonies,　compared　to　control　cells.　The　16　human　prostate　cancer　tissue　samples　revealed　no　clear　upregulation　or　downregulation　in　MLF1IP　gene　expression.　MLF1IP　significantly　promotes　prostate　cancer　cell　proliferation　and　colony　formation　and　significantly　inhibits　apoptosis　without　affecting　cell　cycle　phase　arrest.　Further　study　is　required　to　conclusively　determine　whether　MLF1IP　is　upregulated　in　human　prostate　cancer　tumors　and　to　determine　the　precise　cellular　mechanism(s)　for　MLF1IP　in　prostate　carcinogenesis.