RT Journal Article SR Electronic T1 Lurasidone Sensitizes Cancer Cells to Osimertinib by Inducing Autophagy and Reduction of Survivin JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 4321 OP 4331 DO 10.21873/anticanres.15237 VO 41 IS 9 A1 SHUHEI SUZUKI A1 MASAHIRO YAMAMOTO A1 TOMOMI SANOMACHI A1 KEITA TOGASHI A1 SHIZUKA SEINO A1 ASUKA SUGAI A1 TAKASHI YOSHIOKA A1 MASASHI OKADA A1 CHIFUMI KITANAKA YR 2021 UL http://ar.iiarjournals.org/content/41/9/4321.abstract 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.