Angelica polysaccharides inhibit the growth and promote the apoptosis of U251 glioma cells in vitro and in vivo

Zhang, Wenfeng; Yang, Yan; Li, Xin; Xu, Da-yan; Yan, Yunqi; Gao, Qun; Jia, Ailing; Duan, Minghua

doi:10.1016/j.phymed.2017.06.007

Cited by 24 publications

(13 citation statements)

References 44 publications

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“…Flow cytometry analysis showed AP could increase cell apoptosis. Zhang et al () have reported that AP downregulates Bcl‐2 and increases active caspase‐3 thereby inducing U251 glioma cell apoptosis. The AP‐induced increase of Bax/Bcl‐2 could promote cleavage of caspase‐9, resulting in increase of cleaved caspase‐3.…”

Section: Discussionmentioning

confidence: 99%

“…AP has protective effects on rat osteoarthritis cartilage and interleukin‐1β‐stimulated chondrocytes in vitro (Qin et al, ). Moreover, the anti‐tumor activity of AP has been widely reported in cancer cells, including glioma cells (Zhang et al, ) and breast cancer cells (Zhou et al, ). However, the functional roles of AP in neuroblastoma cells as well the underlying mechanisms remain undefined.…”

Section: Introductionmentioning

confidence: 99%

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Angelica sinensis polysaccharide inhibits proliferation, migration, and invasion by downregulating microRNA‐675 in human neuroblastoma cell line SH‐SY5Y

Yang

Shao

Jiang

et al. 2018

Cell Biology International

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Neuroblastoma is the most common tumor diagnosed in children and infants, with high recurrence and poor prognosis. Angelica sinensis polysaccharide (AP) whose average molecular weight is 72,900 Da possesses various bioactivities. We aimed to explore the effects of AP on neuroblastoma SH-SY5Y cells as well as the underlying mechanisms. Effects of AP on cell viability, proliferation, apoptosis, migration, invasion, and expressions of long noncoding RNA H19 (lncRNA-H19), microRNA (miR)-675, and CD44 were assessed. Then, effects of miR-675 overexpression on AP-treated cells were analyzed. Next, expression of key kinases in the PI3K/AKT and JAK/ STAT pathways was detected. The possible target gene of miR-675 was finally explored. Cell viability was reduced by 200-500 µg/mL AP. Meanwhile, AP repressed cell proliferation, migration, and invasion, but induced apoptosis. Expressions of lncRNA-H19 and miR-675 were upregulated in neuroblastoma cells, and were downregulated by AP. AP was also identified to upregulate CD44. We next found AP affected SH-SY5Y cells through downregulating miR-675. Key kinases in the PI3K/AKT and JAK/STAT pathways were downregulated by AP stimulation, while these downregulations were abrogated by miR-675 overexpression. KIF1B isoform β (KIF1Bβ) is proved to be a target of miR-675. In conclusion, AP was first identified to inhibit proliferation, migration, and invasion but induce apoptosis. Furthermore, AP might repress tumorigenesis of SH-SY5Y cells through miR-675-mediated inactivation of the PI3K/AKT and JAK/STAT pathways. Besides, KIF1Bβ might be a target of miR-675.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Angelica sinensis polysaccharide inhibits proliferation, migration, and invasion by downregulating microRNA‐675 in human neuroblastoma cell line SH‐SY5Y

Yang

Shao

Jiang

et al. 2018

Cell Biology International

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“…Diels, and the combination of the four herbs provides insights into the pathogenesis of lung cancer from the perspective of traditional Chinese medicine. Studies have shown that the active ingredients of the WCF components such as aconitine, ginsenoside Rh2 (Li et al, 2020), ginseng peptide GS9, Rg3 (Wang et al, 2018), emodin, Angelica polysaccharide (Zhang et al, 2017) and Angelica volatile oil have anti-tumor activities and can reverse A B FIGURE 5 | WCF combined DDP affected transplanted tumor structure and ultrastructure. (A) HE staining of section slices of tumor tissue in control, DDP and WCF combined DDP groups, respectively.…”

Section: Discussionmentioning

confidence: 99%

Effect of Wenxia Changfu Formula Combined With Cisplatin Reversing Non-Small Cell Lung Cancer Cell Adhesion-Mediated Drug Resistance

et al. 2020

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Non-small cell lung cancer (NSCLC), the major form of primary lung cancer, is a common cause of cancer-related death worldwide. Cell adhesion-mediated drug resistance (CAM-DR), a form of chemotherapy resistance, has been reported to confer resistance to various chemotherapeutic agents. Integrin b1 signaling plays an important role in CAM-DR and has been proposed as a potential target for NSCLC. Wenxia Changfu Formula (WCF) is a Traditional Chinese Compound Prescription for the intervention treatment of NSCLC combined with cisplatin (DDP). This study aims to investigate the effect and mechanism of WCF combined with DDP in reversing CAM-DR. Firstly, the chemical profile of WCF was characterized by UPLC/Q-TOF-MS analysis. A total of 237 compounds with mzCloud Best Match of greater than 70 were identified by using the online database mzCloud. Secondly, we established A549 three-dimensional(3D) cells cultured in vitro and nude mice xenografts models of the A549 cell line with Integrin b1 overexpression. In vitro, the cell viability, migration and adhesion were measured though MTT Assay, Wound Healing Assay and Cell Adhesion Assay, the Integrin b1 expression of the A549 cells was assessed through immunocytochemistry; in vitro, the transplanted tumor morphology and the colocalization of Integrin b1 and its ligands were tested by HE staining and immunofluorescence. As a result, we found that the combination effectively reduced cell viability, suppressed migration and adhesion, and downregulated the protein level of Integrin b1 in three-dimensional cultured A549 cells. And the combination of WCF with DDP significantly inhibited tumor growth, increased organelle vacuolations and decreased colocalization of Integrin b1 and its ligands including fibulin-2 and laminin. Taken together, our results confirm that the combination of WCF with DDP could reverse the lung cancer CAM-DR through the Integrin b1 signaling pathway.

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“…In addition, we detected the expression of apoptosis-related key proteins. 12 The expression of apoptosis-promoting protein Bax increased obviously, while the expression of anti-apoptosis protein Bcl-2 decreased. We also found that the expression of cleaved caspase 3 and cleaved caspase 8 increased significantly, but the changes of LC3 and p62 ( Figure 3C-J) were not obvious, which indicated that the autophagy of U251 cells 13 was not affected by Baohuoside I.…”

Section: Baohuoside I Induces Human Glioma Cells Apoptosis Not Autophagymentioning

confidence: 97%

<p>Baohuoside I via mTOR Apoptotic Signaling to Inhibit Glioma Cell Growth</p>

Guo¹,

Wang²,

Jiang³

et al. 2020

CMAR

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Introduction Baohuoside I, a novel oncotherapeutic agent, has been reported to have anti-cancer effects on a variety of cancers, but its role in glioma and its molecular mechanism are still unclear. Methods The proliferation of U251 cells was detected by real-time cellular analysis (RTCA), CCK-8, Ki67 immunofluorescence and colony formation assay. The effect of Baohuoside I on the invasion and migration of U251 cells was measured by transwell and scratch tests. The apoptosis of U251 cells was detected by flow cytometry. The expression level of related protein was detected by western blotting. Results Baohuoside I could inhibit the proliferation of human glioma cells and induce apoptosis. Further study showed that the migration and invasion ability of glioma was significantly decreased by Baohuoside I. Western blot revealed the expression of p-AMPKα1 protein was up-regulated, and the expression of p-mTOR and p-S6K was down-regulated after Baohuoside I treatment. Tumorigenesis in nude mice showed that Baohuoside I had an anti-glioma effect in vivo. Conclusion We propose a natural product, which can inhibit the proliferation, invasion and migration of glioma and may be a valuable anti-tumor candidate. The inhibitory effect of Baohuoside I on the glioma is achieved by inducing the apoptosis of the tumor cells, rather than autophagy. In addition, the pathway to induce cell apoptosis of Baohuoside I is to target the mTOR signal.

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Angelica polysaccharides inhibit the growth and promote the apoptosis of U251 glioma cells in vitro and in vivo

Cited by 24 publications

References 44 publications

Angelica sinensis polysaccharide inhibits proliferation, migration, and invasion by downregulating microRNA‐675 in human neuroblastoma cell line SH‐SY5Y

Angelica sinensis polysaccharide inhibits proliferation, migration, and invasion by downregulating microRNA‐675 in human neuroblastoma cell line SH‐SY5Y

Effect of Wenxia Changfu Formula Combined With Cisplatin Reversing Non-Small Cell Lung Cancer Cell Adhesion-Mediated Drug Resistance

<p>Baohuoside I via mTOR Apoptotic Signaling to Inhibit Glioma Cell Growth</p>

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