One could hypothesize, therefore, that alcohol-induced increase in HSPA6 expression may represent stress-associated cellular response disrupting the normal functioning of nuclear speckles and consequently halting splicing. Of note, HSPA6 is mostly known for its involvement in carcinogenesis. Specifically, increased expression of HSPA6 was shown to be associated with a poorer prognosis in hepatocellular carcinoma35, an established alcohol-related cancer3. Even though alcohol is not generally considered to be associated with brain tumors, the trend to a higher incidence of brain tumors in heavy drinkers was detected in meta-analysis36. Since alcohol is associated with some cancers (hepatocellular carcinoma, head and neck squamous cell carcinoma, etc.) and splicing is clearly involved in carcinogenesis37, this study may provide novel mechanistic insight and suggest new directions in studying the possible link between AUD and brain tumors.
