p62 overexpression in breast tumors and regulation by prostate-derived Ets factor in breast cancer cells

Molecular Portrait of Clear Cell Renal Cell Carcinoma: An Integrative Analysis of Gene Expression and Genomic Copy Number Profiling

“…Although the integrative analysis presented here was conducted using a completely different approach from that applied by Beroukhim et al (Beroukhim et al, 2009), both studies identified 12 over-expressed genes located at the 5q peak region (GNB2L1, MGAT1, RUFY, RNF130, MAPK9, CANX, SQSTM1, LTC4S, TBC1D9B, HNRPH1, FLT4). Among them, the ubiquitin-binding protein sequestosome 1 (SQSTM1) was found also in the focal amplification region at 5q35.3 by Chen et al and was reported over-expressed in breast and prostate tumors (Kitamura, 2006;Thompson, 2003). Moreover, we confirmed that, as previously evidenced by Cifola and co-workers (Cifola et al, 2008) and recently confirmed at proteomic level , lyxyl oxidase (LOX) is over-expressed in ccRCC.…”

A fluorescence-microscopic and cytofluorometric system for monitoring the turnover of the autophagic substrate p62/SQSTM1

“…12,13 Hence, a reduction in the abundance of p62 due to its sequestration into autophagosomes (which results from the direct molecular interaction between LC3 and the LIR motif of p62) is interpreted as a sign of increased autophagy. 14 Nonetheless, endogenous p62 is not produced at a constant level, because some conditions of cellular stress lead to the induction of p62 at the transcriptional level, [15][16][17] meaning that the level of p62 proteins is not solely determined by its turnover. This problem can be partially circumvented, by introducing recombinant p62 protein into cells and expressing it under the control of a constitutive promoter (like the one of cytomegalovirus, CMV) while distinguishing it from endogenous p62 by a fusion tag.…”

Hypoxia-activated autophagy accelerates degradation of SQSTM1/p62

“…The expression of p62 is induced by the aggregation of unfolded proteins. This aggregation may be launched by changes in cellular redox state, for example during oxidative stress or the inhibition of proteasomal activity by overload of ubiquitin-proteasome system (UPS) (Kuusisto et al, 2001b;Thompson et al, 2003;Nakaso et al, 2004). Autophagy may be involved in the clearance of such protein aggregates, with p62 playing an active role in the process.…”