Fig 1: SCARA3 increases sensitivity of lung cancer cells to cisplatin via the AKT pathway. A Pearson’s correlation analysis showing half-maximal inhibitory concentration (IC50) values of cisplatin in lung cancer cell lines. B Cell viability was measured for H1299 cells overexpressed with empty vector or Flag-tagged SCARA3 followed by treatment with cisplatin (30 μM) for 24 or 48 h. Data are presented as mean ± SD of three independent experiments. **, P < 0.01; ***, p < 0.001. C Level of cleaved-PARP in H1299 cells overexpressed with empty-vector or Flag-tagged SCARA3 was analyzed by Western blot after treatment with indicated concentration of cisplatin for 24 h. D H1299 cells overexpressed with empty-vector or Flag-tagged SCARA3 were analyzed by Western blot using indicated antibodies after treatment with cisplatin (30 μM) for 0, 2, 4, 8, or 24 h. E Cell viability was measured for empty-vector or Flag-tagged SCARA3 overexpressed H1299 cells after treatment with SC79 (5 μM, AKT activator) and/or SP600125 (30 μM, JNK inhibitor) along with cisplatin (30 μM) treatment. Data are presented as mean ± SD of three independent experiments. ns, not significant; ***, p < 0.001. F Western blot analysis was performed for empty-vector or Flag-tagged SCARA3 overexpressed H1299 cells after treatment with SC79 (5 μM, AKT activator) and/or SP600125 (30 μM, JNK inhibitor) along with cisplatin (30 μM). G Schematic of a model for the main mechanism involved in the tumor suppression function of SCARA3 in lung cancer