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. Author manuscript; available in PMC: 2016 Mar 5.
Published in final edited form as: Cell Rep. 2015 Nov 19;13(9):1895–1908. doi: 10.1016/j.celrep.2015.10.059

Figure 4. Oncocytomas Lack Autophagosomes, Accumulate Autophagy Substrates and Dysfunctional Mitochondria, and Are Primed for Mitophagy.

Figure 4

(A) Human oncocytomas accumulate mitochondria (TOM20) and p62 (autophagy substrate) and lack LC3 puncta (autophagosomes) indicative of autophagy inactivation. Representative IHC for each of the two subtypes with all in Figure S2.

(B) Western blots of indicated mitochondrial and autophagy proteins in normal tissues and oncocytomas. Quantitation of LC3-I/II and p62 levels is shown below.

(C) Oncocytomas have evidence for activation of the fission and the PINK1/PARKIN machinery. Western blots of normal and oncocytoma tissues for indicated proteins. FL, full length; ΔMTS, without mitochondrial translocation sequence.

(D) Primary cultures of oncocytoma cells display autophagy substrate accumulation. In contrast to primary cells derived from NAT (NK159/N144), primary oncocytoma cells (O159/O144) accumulate LC3 and p62 aggregates, mitochondria, glycogen, and lipids, characteristics of autophagy impairment.

(E) Primary cultures of oncocytoma cells (0159/O144) show accumulation of dysfunctional mitochondria with several fold more mitochondrial mass but significantly lower relative membrane potential than normal cell controls NK159 and N144.

(F) Primary oncocytoma cells (O159) have reduced OCR and increased ECAR when provided a fermentable carbon source in comparison to normal control cells (N159).