PT - JOURNAL ARTICLE AU - SHUHEI SUZUKI AU - MASAHIRO YAMAMOTO AU - TOMOMI SANOMACHI AU - KEITA TOGASHI AU - SHIZUKA SEINO AU - ASUKA SUGAI AU - TAKASHI YOSHIOKA AU - MASASHI OKADA AU - CHIFUMI KITANAKA TI - Lurasidone Sensitizes Cancer Cells to Osimertinib by Inducing Autophagy and Reduction of Survivin AID - 10.21873/anticanres.15237 DP - 2021 Sep 01 TA - Anticancer Research PG - 4321--4331 VI - 41 IP - 9 4099 - http://ar.iiarjournals.org/content/41/9/4321.short 4100 - http://ar.iiarjournals.org/content/41/9/4321.full SO - Anticancer Res2021 Sep 01; 41 AB - Background/Aim: Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are key drugs in cancer treatment due to their minor adverse effects and outstanding anticancer effects. However, drugs for overcoming EGFR-TKI resistance are not in clinical use so far. Therefore, to overcome resistance, we focused on lurasidone, a new antipsychotic drug, due to its mild adverse effect profile from the viewpoint of drug repositioning. Materials and Methods: We explored the effects of lurasidone alone or in combination with EGFR-TKI on the growth of osimertinib-resistant cancer cells the anti-apoptotic marker expression such as survivin, and autophagy levels by LC-3B expression. Results: Within a non-toxic concentration range in normal cells, lurasidone and osimertinib combination therapy showed a growth-inhibitory effect in osimertinib-resistant cancer cells in vitro and in vivo. Furthermore, lurasidone decreased survivin expression and mildly induced autophagy. Conclusion: Lurasidone may increase the sensitivity to osimertinib in osimertinib-resistant cancer cells in drug repurposing.