| Autophagy is a cellular lysosomal degradation pathway in which damaged or superfluous protein and organelles are cleared.Post-translational modification of Beclin1 is essential for autophagy induction.Here,we demonstrate that TRIM59,a tripartite motif protein,plays an important role in autophagy regulation.Knocking down TRIM59 induces autophagy mainly through modulating TRAF6 induced K63-linked ubiquitination of Beclin1.Overexpressing TRIM59 blocks the formation of Beclin1-PIK3C3 complex.We further demonstrate that TRIM59 can mediate K48-linked ubiquitination of TRAF6,thus promoting the proteasomal degradation of TRAF6.Apart from this,we also prove that Beclin1 does not affect the proliferation of NSCLC cells,but greatly promotes the migration of NSCLC cells.The protein expression of Beclin1 is higher in most tumor tissue of NSCLC patient samples than those of adjacent normal tissues.Taken together,these findings elucidate a new role for TRIM59 in regulating autophagy and provide new evidence that Beclin1 may have some tumor promoting functions under certain circumstances. |
