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Our laboratory has shown that Beclin 1, an autophagy execution protein, is a haploinsufficient tumor suppressor protein. Monoallelic deletions of beclin 1 are found in the majority of cases of sporadic human breast and ovarian carcinoma, and heterozygous deletion of beclin 1 in mice results in mammary neoplastic lesions, lung adenocarcinomas, hepatocellular carcinomas, and B cell lymphomas. Present studies relating to autophagy and cancer are aimed at: (1) investigating whether the tumor suppressor effects of Beclin 1 are mediated through autophagy; (2) identifying the precise mechanisms by which autophagy functions in negative growth control and tumor suppression; (3) evaluating the role of mutations of other autophagy execution genes in cancer, using gene knockout approaches in mice and mutational analyses of human cancers; (4) investigating the role of autophagy inhibition in oncogenesis mediated by Bcl-2 family members and the Class I/PI3K/Akt signaling pathway; and (5) screening small molecule libraries to identify novel compounds that increase Beclin 1 expression and restore autophagy in tumor cells. (View image) |
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