Shikonin promotes autophagy in BXPC-3 human pancreatic cancer cells through the PI3K/Akt signaling pathway

Shi, Shuqing; Cao, Hongxin

doi:10.3892/ol.2014.2293

Cited by 44 publications

(35 citation statements)

References 20 publications

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“…The suppression of PI3K is also reported to attenuate the uptake of LDL (Michael et al 2015). Through the regulation of NF-B and PI3K-AKT signaling pathways, shikonin inhibits the growth (Shi and Cao 2014;Wang et al 2014b;Tian et al 2015), invasion, and metastasis (Min et al 2011;Chen et al 2014) of cells, although most studies are performed in tumor cells. Through the regulation of NF-B, shikonin also reduces the inflammatory response (Liang et al 2013).…”

Section: Discussionmentioning

confidence: 95%

Shikonin inhibits TNF-α-induced growth and invasion of rat aortic vascular smooth muscle cells

Zhang

et al. 2015

Can. J. Physiol. Pharmacol.

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Shikonin is a naphthoquinone compound extracted from the Chinese herb purple gromwell. Shikonin has broad antibacterial, anti-inflammatory, and antitumor activities. The tumor necrosis factor-α (TNF-α)-induced proliferation and invasion of vascular smooth muscle cells (VSMCs) is an important factor that contributes to atherosclerosis. The effects of shikonin on the proliferation and apoptosis of VSMCs have been reported; however, the function of shikonin on TNF-α-mediated growth and invasion of VSMCs during atherosclerosis remains unclear. In this study, we used Western blot, flow cytometry, real-time quantitative PCR, and enzyme-linked immunosorbent assay to investigate the effect of shikonin on the TNF-α-induced growth and invasion of VSMCs and to determine the underlying mechanism. Our results showed that shikonin inhibits the TNF-α-mediated growth and invasion. Further study revealed that shikonin regulates the activation of nuclear factor kappa B and phosphatidyl inositol 3-kinase signaling pathways; modulates the expression of cyclin D1, cyclin E, B-cell lymphoma 2, and Bax; activates caspase-3 and caspase-9; induces cell cycle arrest; and promotes the apoptosis of VSMCs. Together, our results indicate that shikonin may become a promising agent for the treatment of atherosclerosis and they also establish foundation for the development of anti-atherosclerosis drugs.

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Section: Discussionmentioning

confidence: 95%

Shikonin inhibits TNF-α-induced growth and invasion of rat aortic vascular smooth muscle cells

Zhang

et al. 2015

Can. J. Physiol. Pharmacol.

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“…In this study, LC3 acts as an autophagosome membrane marker and is involved in the formation of the autophagy body. There are two kinds of LC3 protein in cells, including LC3-I and LC3-II, among which LC3-I/II conversion reflects the number of autophagosome [11]. Beclin 1 is also specific gene involved in mammalian autophagy, combined with phospholipids inositol triphosphate-kinase (PI3K), and involved in the formation of autophagosomes.…”

Section: Discussionmentioning

confidence: 99%

The critical role of quercetin in autophagy and apoptosis in HeLa cells

Wang

Zhang

et al. 2015

Tumor Biol.

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In recent years, the effects of quercetin on autophagy and apoptosis of cancer cells have been widely reported, while effects on HeLa cells are still unclear. Here, HeLa cells were subjected to quercetin treatment, and then proliferation, apoptosis, and autophagy were evaluated using MTT, flow cytometry, and MDC staining, respectively. The LC3-I/II, Beclin 1, active caspase-3, and S6K1 phosphorylation were detected using Western blot assay. The ultrastructure of HeLa was observed via transmission electron microscope (TEM). Our findings showed that quercetin can dose-dependently inhibit the growth of HeLa cells. The MDC fluorescence was enhanced with increased concentration of quercetin and hit a plateau at 50 μmol/l. Western blot assay revealed that LC3-I/II ratio, Beclin 1, and active caspase-3 protein were enforced in a dose-dependent method. However, the phosphorylation of S6K1 gradually decreased, concomitant with an increase of autophagy. In addition, TEM revealed that the number of autophagic vacuoles was peaked at 50 μmol/l of quercetin. Besides, interference of autophagy with 3-MA led to proliferation inhibition and increased apoptosis in HeLa cells, accompanied by the decreased LC3-I/II conversion and the increased active caspase-3. In conclusion, quercetin can inhibit HeLa cell proliferation and induce protective autophagy at low concentrations; thus, 3-MA plus quercetin would suppress autophagy and effectively increased apoptosis.

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“…In the BXPC-3 human pancreatic carcinoma cell line, it promotes autophagy through the PI3K/Akt signaling pathway (51). In another human pancreatic carcinoma study, PANC-1, BXPC-3, and ASPC-1 cell lines were employed.…”

Section: Benzoquinonementioning

confidence: 99%

A map describing the association between effective components of traditional Chinese medicine and signaling pathways in cancer cells in vitro and in vivo

Xia

Chen

Zhang

et al. 2014

DD^|^T

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Shikonin promotes autophagy in BXPC-3 human pancreatic cancer cells through the PI3K/Akt signaling pathway

Cited by 44 publications

References 20 publications

Shikonin inhibits TNF-α-induced growth and invasion of rat aortic vascular smooth muscle cells

Shikonin inhibits TNF-α-induced growth and invasion of rat aortic vascular smooth muscle cells

The critical role of quercetin in autophagy and apoptosis in HeLa cells

A map describing the association between effective components of traditional Chinese medicine and signaling pathways in cancer cells in vitro and in vivo

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