MAP30, proteína da Momordica charantia, é agente anti-HIV por modular a expressão de genes virais e celulares envolvidos na patogênese do Sarcoma de Kaposi MAP30, proteína da Momordica charantia, é agente anti-HIV por modular a expressão de genes virais e celulares provocando apoptose e antiproliferação em linfoma relacionado com a AIDS infectados com vírus associado ao sarcoma de Kaposi. MAP30 diminui a expressão da ciclina D viral (vCD), da interleucina-6 viral (vIL-6) e do FLIP viral (vFLIP), genes envolvidos na regulação do ciclo celular, patogênese viral e apoptose. MAP diminui a expressão do egr-1, ATF-2, hsp27, hsp90, IkappaB, mdm2, e Skp1, enquanto aumenta genes relacionados com a apoptose, Bax, CRADD e caspase-3. Desta forma, o MAP30 modula a expressaõ de genes virais e celulares envolvidos na patogênese do Sarcoma de Kaposi Anti-HIV agent MAP30 modulates the expression profile of viral and cellular genes for proliferation and apoptosis in AIDSrelated lymphoma cells infected with Kaposi's sarcomaassociated virus. Sun Y1, Huang PL, Li JJ, Huang YQ, Zhang L, Huang PL, Lee-Huang S. Biochem Biophys Res Commun. 2001 Oct 5;287(4):983-94. Author information 1 Department of Biochemistry, New York University School of Medicine, New York, NY 10016, USA. Abstract The anti-HIV agent MAP30 (Momordica anti-HIV protein, 30 kDa) inhibits the proliferation of BC2, an AIDS-related primary effusion lymphoma (PEL) cell line derived from an AIDS patient. BC2 cells are latently infected with Kaposi's sarcoma-associated herpes virus (KSHV), also known as human herpes virus 8 (HHV8). We examined the effect of MAP30 on the expression of viral and cellular genes in BC-2 during latent and lytic states of the viral life cycle. By Northern analysis and RT-PCR, we found that MAP30 downregulates the expression of viral cyclin D (vCD), viral interleukin-6 (vIL-6), and viral FLIP (vFLIP), genes involved in cell cycle regulation, viral pathogenesis, and apoptosis. By pathway-specific cDNA microarray analysis, we found that BC-2 cells express high levels of egr-1, ATF-2, hsp27, hsp90, IkappaB, mdm2, skp1, and IL-2, cellular genes involved in mitogenesis, tumorigenesis, and inhibition of apoptosis in NFkappaB and p53 signaling pathways. These results define for the first time the specific cellular pathways involved in AIDS-related tumorigenesis and suggest specific novel targets for the treatment. Furthermore, we found that MAP30 downregulates the expression of egr-1, ATF-2, hsp27, hsp90, IkappaB, mdm2, and Skp1, while it upregulates the proapoptotic-related genes Bax, CRADD, and caspase-3. Thus, MAP30 modulates the expression of both viral and cellular genes involved in KS pathogenesis. These results provide valuable insight into the molecular mechanisms of MAP30 anti-KS action and suggest its utility as a therapeutic agent against AIDS-related tumors. PMID:11573962