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Luteolin induces apoptosis in vitro through suppressing the MAPK and PI3K signaling pathways in gastric cancer
Lu, XY (Lu, Xueying); Li, YH (Li, Yanhong); Li, XB (Li, Xiaobo); Aisa, HA (Aisa, Haji Akber)
2017
Source PublicationONCOLOGY LETTERS
ISSN1792-1074
Volume14Issue:2Pages:1993-2000
Abstract

Luteolin, an active component of traditional Chinese medicine, exhibits potential for anti-tumor proliferation; however, the molecular events occurring in such process and the signal transduction pathways involved are currently unknown. Our group previously reported that luteolin inhibited proliferation and induced apoptosis in the gastric cancer cell line BGC-823. The aim of the present study was to investigate the mechanism by which the mitogen-activated protein kinase (MAPK) and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) signaling pathways regulate the apoptosis in vitro of BGC-823 cells following treatment with luteolin. It was observed that luteolin induced apoptosis through the intrinsic pathway by increasing the levels of caspase-3, caspase-9 and cytochrome c, and the ratio of B-cell lymphoma (Bcl)-2 associated X protein (Bax) to Bcl-2. Luteolin suppressed the phosphorylation of extracellular signal-regulated kinase in the MAPK signaling pathway, as well as suppressing the phosphorylation of AKT, PI3K and mechanistic target of rapamycin in the PI3K signaling pathway. In addition, luteolin combined with LY294002 markedly increased the Bax/Bcl-2 ratio, while when combined with U0126, luteolin had less effects on the Bax/Bcl-2 ratio compared with luteolin treatment alone, suggesting that both the MAPK and PI3K signaling pathways are involved in the apoptosis induced by luteolin. Furthermore, luteolin attenuated the MAPK and PI3K signaling pathways by increasing the expression of specific dual-specificity phosphatases and decreasing the expression of chemokine (C-X-C motif) ligand 16 at the messenger RNA level, respectively. Taken together, the present results demonstrate that luteolin is a potential chemotherapeutic agent against gastric cancer by exerting a dual inhibition on the MAPK and PI3K signaling pathways.

KeywordLuteolin Gastric Carcinoma Mapk Pi3k Dusps Cxcl16
DOI10.3892/ol.2017.6380
Indexed BySCI
WOS IDWOS:000407904600110
Citation statistics
Cited Times:8[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.xjipc.cas.cn/handle/365002/5046
Collection省部共建新疆特有药用资源利用重点实验室
资源化学研究室
Corresponding AuthorLi, XB (Li, Xiaobo); Aisa, HA (Aisa, Haji Akber)
Affiliation1.Chinese Acad Sci, Xinjiang Tech Inst Phys & Chem, Key Lab Plant Resources & Chem Arid Zone, 40-1 Beijing Rd, Urumqi 830011, Xinjiang, Peoples R China
2.State Key Lab Basis Xinjiang Indigenous Med Plant, Urumqi 830011, Xinjiang, Peoples R China
3.Xinjiang Normal Univ, Coll Life Sci, Xinjiang Key Lab Special Species Conservat & Regu, Urumqi 830054, Xinjiang, Peoples R China
Recommended Citation
GB/T 7714
Lu, XY ,Li, YH ,Li, XB ,et al. Luteolin induces apoptosis in vitro through suppressing the MAPK and PI3K signaling pathways in gastric cancer[J]. ONCOLOGY LETTERS,2017,14(2):1993-2000.
APA Lu, XY ,Li, YH ,Li, XB ,&Aisa, HA .(2017).Luteolin induces apoptosis in vitro through suppressing the MAPK and PI3K signaling pathways in gastric cancer.ONCOLOGY LETTERS,14(2),1993-2000.
MLA Lu, XY ,et al."Luteolin induces apoptosis in vitro through suppressing the MAPK and PI3K signaling pathways in gastric cancer".ONCOLOGY LETTERS 14.2(2017):1993-2000.
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