Department of Anesthesiology, Medical Center of Anesthesiology and Pain, Jiangxi Province, the First Affiliated Hospital of Nanchang University, No. 17, Yong Wai Zheng Road, Donghu district, 330000, Nanchang, P. R. China.
Department of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
BMC Anesthesiol. 2022 Aug 30;22(1):273. doi: 10.1186/s12871-022-01818-y.
To investigate the effect of lidocaine on the expression of voltage-dependent anion channel 1 (VDAC1) in breast invasive carcinoma (BRCA) and its impact on the apoptosis of breast cancer cells.
We collected clinical data from patients with invasive breast cancer from 2010 to 2020 in the First affiliated hospital of Nanchang University, evaluated the prognostic value of VDAC1 gene expression in breast cancer, and detected the expression of VDAC1 protein in breast cancer tissues and paracancerous tissues by immunohistochemical staining of paraffin sections. Also, we cultured breast cancer cells (MCF-7) to observe the effect of lidocaine on the apoptosis of MCF-7 cells.
Analysis of clinical data and gene expression data of BRCA patients showed VDAC1 was a differentially expressed gene in BRCA, VDAC1 may be of great significance for the diagnosis and prognosis of BRCA patients. Administration of lidocaine 3 mM significantly decreased VDAC1 expression, the expression of protein Bcl-2 was significantly decreased (p < 0.05), and the expression of p53 increased significantly (p < 0.05). Lidocaine inhibited the proliferation of MCF-7 breast cancer cells, increased the percentage of G2 / M phase cells and apoptosis.
Lidocaine may inhibit the activity of breast cancer cells by inhibiting the expression of VDAC1, increasing the apoptosis in breast cancer cells.
探讨利多卡因对乳腺癌中电压依赖性阴离子通道 1（VDAC1）表达的影响及其对乳腺癌细胞凋亡的影响。
我们收集了 2010 年至 2020 年南昌大学第一附属医院浸润性乳腺癌患者的临床资料，评估了 VDAC1 基因表达在乳腺癌中的预后价值，并通过免疫组化染色检测石蜡切片中乳腺癌组织和癌旁组织中 VDAC1 蛋白的表达。此外，我们培养乳腺癌细胞（MCF-7），观察利多卡因对 MCF-7 细胞凋亡的影响。
对 BRCA 患者的临床资料和基因表达数据分析显示，VDAC1 是 BRCA 中的差异表达基因，VDAC1 对 BRCA 患者的诊断和预后可能具有重要意义。给予 3 mM 利多卡因可显著降低 VDAC1 的表达，蛋白 Bcl-2 的表达显著降低（p < 0.05），p53 的表达显著增加（p < 0.05）。利多卡因抑制 MCF-7 乳腺癌细胞的增殖，增加 G2 / M 期细胞和凋亡的比例。
利多卡因可能通过抑制 VDAC1 的表达，增加乳腺癌细胞的凋亡来抑制乳腺癌细胞的活性。
