In MCF7 cell, tumor suppressive function of wild type p53 was restrained by oncogene GTSE1 via downregulating p53 protein level; in MDA-MB-468 cell, mutant homozygote of p53 was able to drive tumorigenesis and GTSE1 promotes cancer process in a p53-independent manner mainly by affecting stability of tubulin or EMT pathway; in MDA-MB-231 cell, GTSE1 can inhibit the function of the wild-type part protein of p53 mutant heterozygotes to promote breast cancer progression in a p53-partially dependent manner. This evidence concerns the gene GTSE1 and breast carcinoma.