Dihydrotestosterone is an endogenous androgen sex steroid and hormone and a potent agonist of the androgen receptor .
In AR-positive bladder cancer UMUC3 and TCC-SUP cells, dihydrotestosterone (DHT) increases the expression of EGFR
and ERBB2 both in mRNA and in protein levels. In AR-positive cell,DHT additionally upregulates the levels of phosphorylation
of EGFR (pEGFR) and its downstream proteins AKT (pAKT) and ERK1/2 (pERK), induced by EGF treatment.
DHT-treated SOD1-G93A mice demonstrate ameliorated muscle atrophy and increased body weight, which is associated with
stronger grip-strength. DHT treatment increases the expression of insulin-like growth factor-1 in muscle, which can exert
myotrophic as well as neurotrophic effects through retrograde transport. DHT treatment attenuates neuromuscular junction
denervation, and axonal and motoneuron loss. DHT-treated SOD1-G93A mice demonstrates improvement in motor behavior
as assessed by rota-rod and gait analyses, and an increased lifespan.