TY - JOUR T1 - Lurasidone Sensitizes Cancer Cells to Osimertinib by Inducing Autophagy and Reduction of Survivin JF - Anticancer Research JO - Anticancer Res SP - 4321 LP - 4331 DO - 10.21873/anticanres.15237 VL - 41 IS - 9 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 Y1 - 2021/09/01 UR - http://ar.iiarjournals.org/content/41/9/4321.abstract N2 - 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. ER -