Abstract
Background/Aim Boric acid (BA) is thought to have anticancer effects, but only a handful of studies tackled this subject. Though a very common compound, little is known about its therapeutic value, mechanisms and effective doses. This study investigates into its therapeutic value and autophagy as a possible mechanism.
Materials and Methods We evaluated the potency of BA treatment in seven different cell lines. We hypothesized that autophagy is involved in the mechanism of BA toxicity in tumor cells based on observations in plants, insects and cancer cell lines. Changes in autophagy-related proteins were measured after BA treatment. Finally, we suspected that blockage of autophagy would increase the effectiveness of BA treatment and enable the use of smaller doses.
Results Our results demonstrate that all studied cell lines did not suffer mortality in low to medium doses of BA (up to 5mM). However, a high dose (over 25mM) could inflict significant death in all cell lines. Those high doses caused P62/SQSTM1 consumption and LC3II-B accumulation after 3 days of treatment. Using small doses of BA in combination with autophagy blockage did not improve cytotoxicity in lung cancer cell lines.
Conclusion We conclude that high concentrations of BA affect autophagy in short-term treatments. Not enough data is available about BA toxicity, so BA use as cancer treatment can be possible if new toxicity studies are performed.
