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Effect of Lidocaine Regulating RhoA/ROCK Axison Biological Behavior of Colorectal Cancer Cells


ZHAO Xin1*, YIN Jian2, JIA Tong3

( 1Department of Anesthesiology, Zhangjiakou Fifth Hospital, Zhangjiakou 075000, China; 2Department of Anesthesiology, Zhangjiakou First Hospital, Zhangjiakou 075000, China; 3Department of Anesthesiology, the First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China)
Abstract:

This study focused on the effects of Lido (lidocaine) on the biological behavior of CRC(colorectal cancer) cells by regulating the RhoA (Ras homologous gene family member A)/ROCK (Rho associated coiled-coil forming protein kinase) axis. In this study, human colorectal cancer cells LS513 were treated with0~1 250 μmol/L lidocaine, and cell viability was detected by CCK-8 method to screen suitable drug concentration.The cells were grouped into Control group, lidocaine low concentration group (Lido-L group, 500 μmol/L Lido),lidocaine medium concentration group (Lido-M group, 750 μmol/L Lido), lidocaine high concentration group(Lido-H group, 1 000 μmol/L Lido) and lidocaine high concentration+ROCK signal pathway activator LPA group (LidoH+LPA group, 1 000 μmol/L Lido+10 μmol/L LPA group). Edu was applied to detect cell proliferation; scratch healing test and transwell chamber test were applied to detect cell migration and invasion ability, respectively; flow cytometry was applied to detect cell apoptosis; Western blot was applied to detect the expression of PCNA, Bax, Bcl2, RhoA, ROCK 1, E-cadherin, and N-cadherin proteins. In this study, compared with 0 μmol/L Lido, the activity ofLS513 cells treated with 500 μmol/L, 750 μmol/L, 1 000 μmol/L and 1 250 μmol/L Lido obviously decreased (P<0.05),lidocaine of 500 μmol/L, 750 μmol/L and 1 000 μmol/L was selected for subsequent experiments. Compared withthe Control group, the Edu positive rate, scratch healing rate, cell invasion number, and PCNA, N-cadherin, Bcl2, RhoA, and ROCK 1 protein expression of LS513 cells in the Lido-L group, Lido-M group, and Lido-H groupdecreased sequentially (P<0.05), the apoptosis rate, E-cadherin and Bax protein expression increased sequentially(P<0.05); compared with the Lido-H group, the Edu positive rate, scratch healing rate, cell invasion number, and PCNA,N-cadherin, Bcl-2, RhoA, and ROCK 1 protein expression of LS513 cells in the Lido-H+LPA group obviously increased(P<0.05), the apoptosis rate, E-cadherin, and Bax protein expression were obviously reduced (P<0.05). Lidocaine mayinhibit the malignant biological behavior of colorectal cancer cells by inhibiting RhoA/ROCK signaling pathway.


CSTR: 32200.14.cjcb.2024.03.0010