The aim of this study is to unravel the role of Cyanidin-3-glucoside (C3G) and its potential mechanisms in lung adenocarcinoma (LUAD). The cell clones, proliferation, apoptosis, migration, and invasion in H1299 and A549 cells were determined by colony formation assay, 5-ethynyl-20 deoxyuridine (EdU) assay, flow cytometry, and transwell assay, respectively. The expression of p53-induced gene 3 (TP53I3) was assessed and the prognostic values of TP53I3 in LUAD via the dataset from the Cancer Genome Atlas (TCGA). In addition, the mRNA and protein expressions were detected by quantitative real-time PCR (qRT-PCR) and western blot. C3G inhibited the proliferation, migration, and invasion of, and also promoted the apoptosis in H1299 and A549 cells. The database of TCGA showed TP53I3 was highly expressed in LUAD tissues and correlated with the poor prognosis of LUAD patients. Moreover, we also found that C3G inhibited the proliferation, migration and invasion, and promoted apoptosis in H1299 and A549 cells by downregulating TP53I3. Additionally, C3G could inhibit the activation of phosphatidylinositol 3′-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in H1299 and A549 cells by downregulating TP53I3. This study demonstrated that C3G could inhibit the proliferation, migration and invasion, and also facilitate the apoptosis through downregulating TP53I3 and inhibiting PI3K/AKT/mTOR pathway in LUAD.

中文翻译：

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Cyanidin-3-glucoside通过下调TP53I3和抑制PI3K/AKT/mTOR通路抑制肺腺癌的进展

本研究的目的是阐明 Cyanidin-3-glucoside (C3G) 的作用及其在肺腺癌 (LUAD) 中的潜在机制。H1299 和 A549 细胞的细胞克隆、增殖、凋亡、迁移和侵袭分别通过集落形成试验、5-乙炔基-20 脱氧尿苷 (EdU) 试验、流式细胞术和 transwell 试验测定。通过癌症基因组图谱 (TCGA) 的数据集，评估了 p53 诱导基因 3 (TP53I3) 的表达以及 LUAD 中 TP53I3 的预后价值。此外，通过定量实时PCR（qRT-PCR）和蛋白质印迹检测mRNA和蛋白质表达。C3G抑制H1299和A549细胞的增殖、迁移和侵袭，并促进其凋亡。TCGA 数据库显示 TP53I3 在 LUAD 组织中高表达，与 LUAD 患者的不良预后相关。此外，我们还发现C3G通过下调TP53I3抑制H1299和A549细胞的增殖、迁移和侵袭，促进细胞凋亡。此外，C3G 可以通过下调 TP53I3 抑制 H1299 和 A549 细胞中磷脂酰肌醇 3'-激酶 (PI3K)/蛋白激酶 B (AKT)/哺乳动物雷帕霉素靶标 (mTOR) 通路的激活。本研究表明C3G可以抑制LUAD的增殖、迁移和侵袭，并通过下调TP53I3和抑制PI3K/AKT/mTOR通路促进细胞凋亡。并通过下调 TP53I3 促进 H1299 和 A549 细胞凋亡。此外，C3G 可以通过下调 TP53I3 抑制 H1299 和 A549 细胞中磷脂酰肌醇 3'-激酶 (PI3K)/蛋白激酶 B (AKT)/哺乳动物雷帕霉素靶标 (mTOR) 通路的激活。本研究表明C3G可以抑制LUAD的增殖、迁移和侵袭，并通过下调TP53I3和抑制PI3K/AKT/mTOR通路促进细胞凋亡。并通过下调 TP53I3 促进 H1299 和 A549 细胞凋亡。此外，C3G 可以通过下调 TP53I3 抑制 H1299 和 A549 细胞中磷脂酰肌醇 3'-激酶 (PI3K)/蛋白激酶 B (AKT)/哺乳动物雷帕霉素靶标 (mTOR) 通路的激活。本研究表明C3G可以抑制LUAD的增殖、迁移和侵袭，并通过下调TP53I3和抑制PI3K/AKT/mTOR通路促进细胞凋亡。