Ubiquilin (UBQLN) proteins are adaptors thought to link ubiquitinated proteins 
to the proteasome. However, our lab has recently reported a previously 
unappreciated role for loss of UBQLN in lung cancer progression. In fact, UBQLN 
genes are lost in over 50% of lung cancer samples examined. However, a reason 
for the loss of UBQLN has not been proposed, nor has a selective pressure that 
could lead to deletion of UBQLN been reported. Diesel Exhaust Particles (DEP) 
are a major concern in the large cities of developing nations and DEP exposed 
populations are at an increased risk of developing a number of illnesses, 
including lung cancer. A connection between DEP and UBQLN has never been 
examined. In the present study, we determined the effect of DEP on lung cell 
lines and were interested to determine if UBQLN proteins could potentially play 
a protective role following treatment with DEP. Interestingly, we found that DEP 
treated cells have increased expression of UBQLN proteins. In fact, 
over-expression of UBQLN was capable of protecting cells from DEP toxicity. To 
investigate the mechanism by which DEP leads to increased UBQLN protein levels, 
we identified and interrogated microRNAs that were predicted to regulate UBQLN 
mRNA. We found that DEP decreases the oncogenic microRNA, MIR155. Further, we 
showed that MIR155 regulates the mRNA of UBQLN1 and UBQLN2 in cells, such that 
increased MIR155 expression increased cell invasion, migration, wound formation 
and clonogenicity in UBQLN-loss dependent manner. This is the first report of an 
environmental carcinogen regulating expression of UBQLN proteins. We show that 
exposure of cells to DEP causes an increase in UBQLN levels and that MIR155 
regulates mRNA of UBQLN. Thus, we propose that DEP-induced repression of MIR155 
leads to increased UBQLN levels, which in turn may be a selective pressure on 
lung cells to lose UBQLN1.