Salidroside inhibited the proliferation of gastric cancer cells through up-regulating tumor suppressor miR-1343-3p and down-regulating MAP3K6/MMP24 signal molecules.

IF 5.4 3区 材料科学 Q2 CHEMISTRY, PHYSICAL ACS Applied Energy Materials Pub Date : 2024-12-31 Epub Date: 2024-03-04 DOI:10.1080/15384047.2024.2322206
Xiaoping Wang, Zhendong Zhang, Xiaolan Cao
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Abstract

Salidroside inhibited the proliferation of cancer cell. Nevertheless, the mechanism has not been completely clarified. The purpose of the study is to explore the mechanisms of salidroside against gastric cancer. To analyze the changes of microRNA (miRNA) in gastric cancer cells under the treatment of salidroside, the miRNA expression was analyzed by using RNA-seq in cancer cells for 24 h after salidroside treatment. The differentially expressed miRNAs were clustered and their target genes were analyzed. Selected miRNA and target mRNA genes were further verified by q-PCR. The expressions of target genes in cancer cells were detected by immunohistochemistry. Cancer cell apoptotic index was significantly increased after salidroside treatment. The proliferation of gastric cancer cells were blocked at S-phase cell cycle. The expression of 44 miRNAs changed differentially after salidroside treatment in cancer cells. Bioinformatic analysis showed that there were 1384 target mRNAs corresponding to the differentially expressed miRNAs. Surprisingly, salidroside significantly up-regulated the expression of tumor suppressor miR-1343-3p, and down-regulated the expression of MAP3K6, STAT3 and MMP24-related genes. Salidroside suppressed the growth of gastric cancer by inducing the cancer cell apoptosis, arresting the cancer cell cycle and down-regulating the related signal transduction pathways. miRNAs are expressed differentially in gastric cancer cells after salidroside treatment, playing important roles in regulating proliferation and metastasis. Salidroside may suppress the growth of gastric cancer by up-regulating the expression of the tumor suppressor miR-1343-3p and down-regulating the expression of MAP3K6 and MMP24 signal molecules.

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水杨梅苷通过上调肿瘤抑制因子miR-1343-3p和下调MAP3K6/MMP24信号分子抑制胃癌细胞的增殖。
水杨甙能抑制癌细胞的增殖。然而,其机制尚未完全阐明。本研究的目的是探索柳氮磺吡啶对抗胃癌的机制。为了分析微RNA(miRNA)在柳氮磺胺吡啶治疗下在胃癌细胞中的变化,研究人员采用RNA-seq技术分析了柳氮磺胺吡啶治疗后24小时内癌细胞中miRNA的表达情况。对差异表达的 miRNA 进行聚类并分析其靶基因。选定的 miRNA 和靶 mRNA 基因通过 q-PCR 进一步验证。免疫组化法检测了靶基因在癌细胞中的表达。经柳氮磺胺吡啶处理后,癌细胞凋亡指数明显增加。在 S 期细胞周期,胃癌细胞的增殖被阻断。44个miRNAs的表达在经柳氮磺胺吡啶处理后发生了不同程度的变化。生物信息学分析表明,有1384个靶mRNA与表达不同的miRNA相对应。令人惊讶的是,水杨甙能显著上调抑癌基因miR-1343-3p的表达,下调MAP3K6、STAT3和MMP24相关基因的表达。通过诱导癌细胞凋亡、阻滞癌细胞周期和下调相关信号转导通路来抑制胃癌的生长。miRNAs在经柳氮苷治疗后的胃癌细胞中表达不同,在调控细胞增殖和转移中发挥重要作用。水杨甙可通过上调抑癌基因miR-1343-3p的表达,下调MAP3K6和MMP24信号分子的表达来抑制胃癌的生长。
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来源期刊
ACS Applied Energy Materials
ACS Applied Energy Materials Materials Science-Materials Chemistry
CiteScore
10.30
自引率
6.20%
发文量
1368
期刊介绍: ACS Applied Energy Materials is an interdisciplinary journal publishing original research covering all aspects of materials, engineering, chemistry, physics and biology relevant to energy conversion and storage. The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrate knowledge in the areas of materials, engineering, physics, bioscience, and chemistry into important energy applications.
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