Ultrasound irradiation inhibits proliferation of cervical cancer cells by initiating endoplasmic reticulum stress-mediated apoptosis and triggering phosphorylation of JNK

BACKGROUND Cervical cancer is the 2nd most frequently diagnosed gynecological cancer. Therefore, it clinically significant to discover an effective anti-cancer approach. OBJECTIVES This study aimed investigate effects of low-intensity ultrasound irradiation (USI) on cervical cells and associated mechanisms cell death. MATERIAL AND METHODS Normal human HaCaT lines C33A, Hela Siha were cultured γ-rays applied at a dosage 2.0 Gy/min. The MTT assay was then used assess viability (proliferation) HaCaT, Hela, cells. Small interfering RNA (siRNA) sequences that silence glucose-related protein (GRP78) gene synthesized. Structural changes exposed USI observed with scanning electron microscopy. Immunocytochemistry western blotting utilized examine GRP78, C/EBP-homologous (CHOP), phosphorylated JNK (p-JNK), caspase-12 expression in RESULTS Ultrasound reduced increased apoptosis, compared untreated tumor (p < 0.05). effect not apparent also induced formation apoptotic bodies 0.05), activated endoplasmic reticulum (ER) stress-associated apoptosis by triggering CHOP expression. Moreover, triggered ER stress upregulating GRP78 Remarkably, phosphorylation initiated increasing Silencing further enhanced CONCLUSIONS significantly inhibited proliferation initiating signaling pathways JNK.