Disease relevance of SART3

• CONCLUSIONS: The SART3 antigen could be an appropriate target molecule for specific immunotherapy for colorectal carcinoma patients [1].
• We have recently shown that Tip110 functions to potentiate the transactivation activity of human immunodeficiency virus type I (HIV-1) Tat protein [2].
• Taken together, these results indicate that Tip110 is a negative regulator of AR transcriptional activation, and may be directly involved in AR-related developmental, physiological, and pathological processes [2].
• Expression of the SART3 tumor rejection antigen in renal cell carcinoma [3].
• SART3 derived peptides at positions 109-118 and 315-323 induced HLA-A24 restricted CTLs that reacted to breast cancer cells from the peripheral blood mononuclear cells (PBMCs) of breast cancer patients [4].

High impact information on SART3

• The NH2-terminal HAT domain of SART3/p110 was necessary and sufficient for specific protein targeting to CBs [5].
• Tip110 bound to AR in an NR box-dependent manner and inhibited AREs-mediated reporter gene expression [2].
• In agreement with these findings, Tip110 overexpression blocked the prostate-specific antigen (PSA) gene, a well characterized target gene of AR from expression in LNCaP cells [2].
• Moreover, knock-down of the constitutive Tip110 expression significantly augmented AR transcriptional activation [2].
• In vivo binding of Tip110 with Tat was confirmed by immunoprecipitation and Western blotting, in combination with mutagenesis [6].

Anatomical context of SART3

• We recently reported the four tumor-rejection antigens (SART1(259), SART2, SART3, and ART4) that possess tumor epitopes capable of inducing HLA-A2402-restricted cytotoxic T lymphocytes (CTLs) in cancer patients [7].
• RESULTS: The 140 kD SART3 antigen was expressed in both the cytosol and nuclear fractions of all six colon carcinoma cell lines, 27 of 41 (65.9%) cytosol fractions, 30 of 41 (73.2%) nuclear fractions of colorectal carcinoma tissue samples, and in 0 of 7 non-tumorous tissues [1].
• The HLA-A2-restricted and tumor-specific CTL line recognized COS-7 cells co-transfected with the SART3 gene and either HLA-A0201, -A0206 or -A0207 cDNA but not those co-transfected with the SART3 gene and HLA-A2402 or -A2601 cDNA [8].
• SART3 was detected on the cell surface of several B-lineage leukemic cells with different maturation stages, but not on normal peripheral blood B cells [9].

Other interactions of SART3

• Our results indicate that the HSA12 evolutionary breakpoint occurs between STAB2 and SART3 in a region spanning less than five million basepairs [10].
• Both SART3 and ART4 antigens were detectable in the majority of these gynecologic cancers tested [7].
• A mutation in SART3 gene in a Chinese pedigree with disseminated superficial actinic porokeratosis [11].
• Oral cancer cell lines had the ability to stimulate IFN-gamma production by the HLA-A24-restricted and SART3-specific CTLs that were established from the peripheral blood mononuclear cells (PBMCs) of an esophageal cancer patient [12].

Analytical, diagnostic and therapeutic context of SART3

• Therefore, these four antigens and their peptides, including SART3 peptides, would be appropriate molecules for use in specific immunotherapy of HLA-A24(+) gynecologic cancer patients [7].
• METHODS: The SART2 and SART3 antigens were investigated by Western blotting in colorectal carcinoma cell lines and in cancer tissues [1].
• Northern blot analysis showed that Tip110 mRNA was expressed in a variety of human tissues and cells [6].
• Induction of cellular immune responses to tumor cells and peptides in colorectal cancer patients by vaccination with SART3 peptides [13].
• 2. By sequence analysis, we found a Val591Met mutation in SART3 in all affected individuals of the family [11].

References