Investigates autophagy's role in ovarian cancer outcomes, suggesting therapy implications.
Despite extensive research, the treatment of ovarian cancer remains a significant challenge. One promising strategy involves the regulation of autophagy in cancer cells. However, this process is exceptionally complex and, depending on numerous factors, it can either suppress tumor progression, by maintaining genomic stability and limiting inflammatory responses, or exert a pro-tumor effect, enabling cancer cells to survive in unfavorable environmental conditions. Furthermore, the activation of this pathway can contribute to the development of resistance to drugs used in ovarian cancer therapy, such as cisplatin or paclitaxel. Current therapeutic approaches focus on both the induction and inhibition of autophagy, primarily by targeting the two most important pathways regulating this process: PI3K/Akt/mTOR and AMPK.
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Zoń et al. (2026) studied this question.
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