Proliferation Effect of Compound Phyllanthus Urinsria Ⅱ and Insulin-like Growth Factor-1 Receptor Signaling Transcription

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Proliferation Effect of Compound Phyllanthus Urinsria Ⅱ and Insulin-like Growth Factor-1 Receptor Signaling Transcription

更新时间：2024-01-04

- Proliferation Effect of Compound Phyllanthus Urinsria Ⅱ and Insulin-like Growth Factor-1 Receptor Signaling Transcription
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 14, Pages: 108-114(2018)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20181316
  CLC： R285.5
- Published：2018
- 稿件说明：
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CHEN Bin, GUO Jie-wen, HE Su, et al. Proliferation Effect of Compound Phyllanthus Urinsria Ⅱ and Insulin-like Growth Factor-1 Receptor Signaling Transcription[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(14): 108-114.
DOI：

CHEN Bin, GUO Jie-wen, HE Su, et al. Proliferation Effect of Compound Phyllanthus Urinsria Ⅱ and Insulin-like Growth Factor-1 Receptor Signaling Transcription[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(14): 108-114. DOI： 10.13422/j.cnki.syfjx.20181316.

摘要

目的：观察叶下珠复方Ⅱ号(CPU Ⅱ)对肝癌Huh7细胞增殖以及叶下珠复方Ⅱ号对胰岛素样生长因子-1受体(IGF-1R)信号通路转录的影响，探讨叶下珠复方Ⅱ号抗肝癌作用机制。方法：采用小分子干扰RNA技术(siRNA)转染肝癌Huh7细胞，构建抑制IGF-1R的肝癌Huh7细胞(anti-IGF-1R Huh7)，选择稳定表达的抑制IGF-1R的肝癌Huh7细胞，将肝癌Huh7细胞以及抑制IGF-1R的肝癌Huh7细胞分别分为4组：空白组，叶下珠复方Ⅱ号高、低质量浓度组(3.0，1.5 g·L-1)以及5-氟尿嘧啶(5-FU)组(0.03 g·L-1)，采用噻唑蓝(MTT)比色法测定药物对各组细胞增殖的影响，通过实时荧光定量PCR(Real-time PCR)以及蛋白免疫印迹法(Western blot)检测IGF-1R以及其下游相关指标mRNA及蛋白表达。结果：与空白组比较，转染(SASI_Hs01_00126196及SASI_Hs01_00126196_AS)序列肝癌Huh7 IGF-1R mRNA及蛋白表达量最低，选择该细胞进行实验。MTT比色实验结果表明，与空白组比较，叶下珠复方Ⅱ号能够抑制Huh7细胞以及抑制IGF-1R的肝癌Huh7细胞增殖，并且siRNA抑制IGF-1R基因表达后，叶下珠复方Ⅱ号还能继续抑制Huh 7细胞增殖，且IGF-1R，磷脂酰肌醇3-激酶(PI3K)和丝氨酸-苏氨酸蛋白激酶3(Akt3) mRNA表达量进一步下降(P < 0.05)。结论：叶下珠复方Ⅱ号能够抑制Huh7细胞增殖，作用机制可能是抑制IGF-1R及其下游mRNA转录有关。

Abstract

Objective: To observe the effect of compound phyllanthus urinsria Ⅱ (CPU Ⅱ) on the proliferation of hepatocellular carcinoma Huh7 cells and the transcription of insulin-like growth factor-1 receptor (IGF-1R) signaling pathway

and explore the mechanism of action of CPU Ⅱ in inhibiting liver cancer. Method: Small interfering RNA (siRNA) was transfected into Huh7 cells to construct hepatocellular carcinoma Huh7 cells that inhibited insulin-like growth factor-1 receptor (anti-IGF-1R Huh7). IGF-1R Huh7 cells with stable expression

namely Huh7 cells of hepatocellular carcinoma and Huh7 cells of hepatocellular carcinoma that inhibited insulin-like growth factor-1 receptor

were divided into four groups:control group

high and low-dose CPU Ⅱ groups (3.0

1.5 g·L-1) and 5-fluorouracil(5-FU) (0.03 g·L-1). The effect of drugs on the proliferation of each group were determined by methylthiazolyl tetrazolium(MTT)assay. Real-time PCR was used to detect the mRNA expression of IGF-1R and its downstream genes. Result: The mRNA expression of Huh7 IGF-1R and the lowest expression level of Huh7 were detected by Real-time PCR and Western blot. The cells were selected for experiment. The results of MTT showed that CPU Ⅱ could inhibit the proliferation of Huh7 cells and Huh7 cells that inhibit IGF-1R; after siRNA inhibited IGF-1R gene expression

CPU Ⅱ could continue the proliferation of Huh 7 cells; and the mRNA expressions of IGF-1R

Phosphatidylinositol 3-kinase (PI3K)and Serine-threonine protein kinase 3(Akt)further decreased compared with the control group (P<0.05). Conclusion: CPU Ⅱ can inhibit the proliferation of Huh7 cells. The mechanism may be related to the inhibition of IGF-1R and its downstream mRNA transcription.

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