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Proposed mechanism for ABHD5 in regulating autophagy and tumorigenesis of colon cancer. ABHD5 physically interacts with BECN1 to competitively occupy the cleavage sites of BECN1 with CASP3. In the absence of ABHD5, CASP3 acquires an advantage to cleave BECN1, consequently impairing BECN1-induced autophagic flux. The defective autophagy in ABHD5-deficient cells augments DNA damage and genomic instability, thus promoting tumorigenesis.
