Jichu yixue yu linchuang (Mar 2022)

Ropivacaine inhibits proliferation, migration and invasion of human liver cancer cell line Hep3B

  • SUN Quan-peng, FAN Chao, ZHAN De-xi, FAN Yi-ming, SUN Wei-feng

DOI
https://doi.org/10.16352/j.issn.1001-6325.2022.03.025
Journal volume & issue
Vol. 42, no. 3
pp. 448 – 453

Abstract

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Objective To study the effects of ropivacaine on the biological behaviour of liver cancer cell line Hep3B and to explore its molecular mechanism. Methods Hep3B cells were divided into the control group, ropivacaine group, si-NC group, si-LINC00853 group, pcDNA-NC group, pcDNA-LINC00853 group,(ropivacaine+pcDNA-NC) group and (ropivacaine +pcDNA-LINC00853) group. Cell Counting Kit(CCK-8), Transwell assays, and RT-qPCR were applied to detect cell proliferation, migration, invasion and LINC00853 expression. Western blot was used to analyze the expression of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 2(MMP2) and MMP9 proteins. Results Compared with the NC group, the proliferation inhibition rate of Hep3B cells in the ropivacaine group was elevated, cell migration and invasion were inhibited. The expression of PCNA, MMP2, MMP9 and LINC00853 was reduced (P＜0.05). Compared with the si-NC group, the proliferation inhibition rate of Hep3B cells in the si-LINC00853 group was elevated, cell migration and invasion were reduced and the expression of PCNA, MMP2, MMP9 protein was decreased (P＜0.05). Compared with the pcDNA-NC group, the proliferation inhibition of Hep3B cells in the pcDNA-LINC00853 group was reduced, cell migration and invasion were increased. The expression of PCNA, MMP2, and MMP9 protein was increased (P＜0.05). Compared with the (ropivacaine+ pcDNA-NC) group, the proliferation inhibitio of Hep3B cells in the (ropivacaine+ pcDNA-LINC00853) group was reduced, cell migration and invasion were increased and the expression of PCNA, MMP2 and MMP9 protein increased (P＜0.05). Conclusions Ropivacaine can inhibit liver cancer cell line Hep3B proliferation, migration and invasion. Its mechanism may be related to the down-regulation of LINC00853 expression.

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