The antitumor effect of tanshinone IIA on anti-proliferation and decreasing VEGF/VEGFR2 expression on the human non-small cell lung cancer A549 cell line

Xie, Jun; Liu, Jiahui; Liu, Heng; Liang, Shihui; Lin, Mei-Gui; Gu, Yue-Yu; Liu, Taoli; Wang, Dongmei; Ge, Hui

doi:10.1016/j.apsb.2015.07.008

Cited by 96 publications

(71 citation statements)

References 28 publications

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“…Wang et al [27] verified that Tan IIA could suppress the growth and promote the apoptosis of esophageal cancer cells possibly through impacting the cell cycle and apoptotic signaling pathways . Furthermore, Xie et al [28] illustrated that Tan IIA could inhibit the proliferation of non-small cell lung carcinoma cells, induce apoptosis and arrest cell cycle in the S phase, and the corresponding mechanism might be that Tan IIA inhibits angiogenesis by targeting VEGF/VEGFR2 protein kinase domains.…”

Section: Discussionmentioning

confidence: 99%

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Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

Ding

Wang²,

Wang³

et al. 2016

Pharmacology

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Objective: To test the effects of Tanshinone IIA (Tan IIA) on cell viability, cycle, apoptosis, and autophagy of human glioma cell U251 by regulating phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signal pathway. Methods: Tan IIA and PI3K agonist (740 Y-P) were used to treat glioma cells U251. MTT assay was used to assess cell viability and flow cytometry was used to detect cell apoptosis and cell cycle. The expressions of apoptosis-related proteins (Bcl-2 and Bax), autophagy-related proteins (LC3B and Beclin 1) and PI3K/Akt/mTOR signal pathway-associated proteins (p-PI3K, p-Akt and p-mTOR) were evaluated by Western blotting. Results: Tan IIA decreased the expression of p-PI3K and p-Akt proteins, inhibited cell viability and promoted apoptosis. Meanwhile, the expression of Bax increased, while the expression of Bcl-2 decreased. In addition, Tan IIA promoted autophagy in U251 glioma cells and raised the expression of LC3B and Beclin 1. However, 740 Y-P played a reversed role of Tan IIA in cell viability, cycle, apoptosis, and autophagy of U251 cells. Conclusion: Tan IIA could suppress the viability of U251 cells and induce cell apoptosis and autophagy, which might be related to the inhibition of the PI3K/Akt/mTOR signal pathway.

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Section: Discussionmentioning

confidence: 99%

“…However, there were a few studies that investigated the anti-tumor effect of Tan IIA on glioma [28][29][30] . Yang et al [31] demonstrated that Tan IIA could inhibit the proliferation and promote apoptosis of glioma stem cells, and this finding was consistent with our results.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

Ding

Wang²,

Wang³

et al. 2016

Pharmacology

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“…Our previous studies showed that tanshinone IIA inhibited the growth of NSCLC A549 cell line by decreasing VEGF/VEGFR2 expression [12]. It has been documented that the combination of tanshinone IIA and ADM not only could exhibit a synergistic effect on HepG2, but also improve the cytotoxicity of ADM with less cardiotoxicity [9].…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA combined with adriamycin inhibited malignant biological behaviors of NSCLC A549 cell line in a synergistic way

Xie

Liu

et al. 2016

BMC Cancer

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BackgroundThe study was designed to develop a platform to verify whether the extract of herbs combined with chemotherapy drugs play a synergistic role in anti-tumor effects, and to provide experimental evidence and theoretical reference for finding new effective sensitizers.MethodsInhibition of tanshinone IIA and adriamycin on the proliferation of A549, PC9 and HLF cells were assessed by CCK8 assays. The combination index (CI) was calculated with the Chou-Talalay method, based on the median-effect principle. Migration and invasion ability of A549 cells were determined by wound healing assay and transwell assay. Flow cytometry was used to detect the cell apoptosis and the distribution of cell cycles. TUNEL staining was used to detect the apoptotic cells. Immunofluorescence staining was used to detect the expression of Cleaved Caspase-3. Western blotting was used to detect the proteins expression of relative apoptotic signal pathways. CDOCKER module in DS 2.5 was used to detect the binding modes of the drugs and the proteins.ResultsBoth tanshinone IIA and adriamycin could inhibit the growth of A549, PC9, and HLF cells in a dose- and time-dependent manner, while the proliferative inhibition effect of tanshinone IIA on cells was much weaker than that of adriamycin. Different from the cancer cells, HLF cells displayed a stronger sensitivity to adriamycin, and a weaker sensitivity to tanshinone IIA. When tanshinone IIA combined with adriamycin at a ratio of 20:1, they exhibited a synergistic anti-proliferation effect on A549 and PC9 cells, but not in HLF cells. Tanshinone IIA combined with adriamycin could synergistically inhibit migration, induce apoptosis and arrest cell cycle at the S and G2 phases in A549 cells. Both groups of the single drug treatment and the drug combination up-regulated the expressions of Cleaved Caspase-3 and Bax, but down-regulated the expressions of VEGF, VEGFR2, p-PI3K, p-Akt, Bcl-2, and Caspase-3 protein. Compared with the single drug treatment groups, the drug combination groups were more statistically significant. The molecular docking algorithms indicated that tanshinone IIA could be docked into the active sites of all the tested proteins with H-bond and aromatic interactions, compared with that of adriamycin.ConclusionsTanshinone IIA can be developed as a novel agent in the postoperative adjuvant therapy combined with other anti-tumor agents, and improve the sensibility of chemotherapeutics for non-small cell lung cancer with fewer side effects. In addition, this experiment can not only provide a reference for the development of more effective anti-tumor medicine ingredients, but also build a platform for evaluating the anti-tumor effects of Chinese herbal medicines in combination with chemotherapy drugs.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2921-x) contains supplementary material, which is available to authorized users.

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“…Vasculogenesis refers to the process of differentiation and proliferation of endothelial progenitor cells (EPCs) at tumor sites. Angiogenesis refers to endotheliosis and the formation of new blood vessels at or around tumor sites using the original blood vessels as a template (15). Some studies have shown that bone marrow-derived EPCs in adults are involved in the formation of new blood vessels, which challenges current models in which angiogenesis only occurs during embryonic development.…”

Section: Introductionmentioning

confidence: 99%

Involvement of breast cancer stem cells in tumor angiogenesis

Wang

et al. 2017

Oncol Lett

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Abstract. The aim of the present study was to investigate the role of breast cancer stem cells (BCSCs) in the angiogenesis of breast cancer tumors. The expression levels of mutant p53, cluster of differentiation (CD)31, vascular endothelial factor (VEGF), in addition to human epidermal growth factor (HER)2, were detected in the blood vessels of human breast cancer (BC) tissue samples. CD44 + /CD24 -/low cells were selected from single-cell suspensions of BC tissues to assess the expression of CD31 and CD105, in addition to the ability of these cells to metabolize acetylated low-density lipoprotein (Ac-LDL). Furthermore, vascular-like structures were observed histologically. Mutant p53, CD31 and VEGF were all expressed in these tissues. CD44+ cells comprised 7.5±2.6 and 94.3±4.7% of the cell population prior to and following sorting, respectively. CD24 + cells comprised 48.2±9.4 and 4.3±4% of the cell population prior to and following sorting, respectively. A low proportion of CD24 + cells corresponded to a high proportion of CD24 -/low cells. The percentages of CD105 + and CD31 + glomus cells in the mammary gland were 4.5±0.9 and 6.2±1.3%, respectively, and following passaging for three generations, these increased to 79.6±9.3 and 84.1±10.7%, respectively (P<0.05). Cells were cultured using an endothelial cell culture system, and they internalized DiL-Ac-LDL. Here, vascular endothelial cells formed vascular-like structures, whereas the control group demonstrated no such structures. Overall, the results suggest that BCSCs-derived endothelial cells may contribute to tumor angiogenesis.

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The antitumor effect of tanshinone IIA on anti-proliferation and decreasing VEGF/VEGFR2 expression on the human non-small cell lung cancer A549 cell line

Cited by 96 publications

References 28 publications

Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

Tanshinone IIA combined with adriamycin inhibited malignant biological behaviors of NSCLC A549 cell line in a synergistic way

Involvement of breast cancer stem cells in tumor angiogenesis

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