Mechanistically, it is found that overexpression of SAMD4A in breast cancer cells downregulates the expression of proangiogenic genes including CXCL5, ENG, IL1β and ANGPT1, and destabilizes the proangiogenic mRNAs by the SAM domain of SAMD4A directly binding to the conserved stem-loop structure in the 3’-UTR of these mRNAs, which leads to inhibition of breast tumor angionegesis and progression. Here, SAMD4A is linked to breast neoplasm.