Angelicin inhibits human lung carcinoma A549 cell growth and migration through regulating JNK and ERK pathways

Li, Guangcai; He, Yuan; Yao, Jun; Huang, Chuying; Song, Xiusheng; Deng, Yan; Xie, Sheng; Ren, Jie; Jin, Meng; Liu, Huiguo

doi:10.3892/or.2016.5166

Cited by 28 publications

(36 citation statements)

References 29 publications

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“…Mmp9 is regulated by NF-B signalling, which has been associated with poor prognosis in non-small cell lung cancers (25). Mmp9 inhibition has been reported to attenuate cancer cell invasion and metastasis (26,27). We found an increased expression of syndecan-2, NF-B (p65) and mmp9 in lung adenocarcinoma tissue ( Figure E2).…”

Section: Syndecan-2 Increases Mmp9 Expression and Activity And Is Assmentioning

confidence: 71%

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Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness

Tsoyi

Osorio

Fernandez

et al. 2019

Am J Respir Cell Mol Biol

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Rationale: Altered expression of syndecan-2, a heparan sulfate proteoglycan, has been associated with diverse types of human cancers. However, the mechanisms by which syndecan-2 may contribute to the pathobiology of lung adenocarcinoma have not been previously explored. Methods: Syndecan-2 levels were measured in human lung adenocarcinoma samples and Lung Cancer Tissue Microarrays using immunohistochemistry and real time-PCR. To understand the role of syndecan-2 in vitro, SDC2 was silenced or overexpressed in A549 lung adenocarcinoma cells. The invasive capacity of cells was assessed using Matrigel invasion assays and measuring matrix metalloproteinase 9 (mmp9) expression. Finally, we assessed tumor growth and metastasis of SDC2-deficient A549 cells in a xenograft tumor model. Results: Syndecan-2 expression was upregulated in malignant epithelial cells and macrophages obtained from human lung adenocarcinomas. Silencing of SDC2 decreased mmp9 expression and attenuated the invasive capacity of A549 lung adenocarcinoma cells. The inhibitory effect of SDC2 silencing on mmp9 expression and cell invasion was reversed by overexpression of mmp9 and syntenin-1. SDC2 silencing attenuated NF-κB p65 subunit nuclear translocation and its binding to the MMP9 promoter, which were restored by overexpression of syntenin-1. SDC2 silencing in vivo reduced tumor mass volume and metastasis. Conclusions: These findings suggest that syndecan-2 plays an important role in the invasive properties of lung adenocarcinoma cells and that its effects are mediated by syntenin-1. Thus, inhibiting syndecan-2 expression or activity could serve as a potential therapeutic target to treat lung adenocarcinoma.

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Section: Syndecan-2 Increases Mmp9 Expression and Activity And Is Assmentioning

confidence: 71%

“…Mmp9, also known as gelatinase B, has been shown to play a prominent role in tumor malignant potential and lung-specific metastasis (23,35). Higher levels of mmp9 are correlated with poor patient prognosis in non-small cell lung cancer (36), and mmp9 inhibition has been reported to attenuate cancer cell invasion and metastasis (26,27).…”

Section: Discussionmentioning

confidence: 99%

Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness

Tsoyi

Osorio

Fernandez

et al. 2019

Am J Respir Cell Mol Biol

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“…However, combined treatment angelicin (50–100 μM) and TRAIL (50 ng/mL) caused apoptotic cell death in Caki, Sk‐hep1, and MDA‐MB‐361 cells, but not normal cells. Li et al () also reported that angelicin inhibited growth and migration via regulation of JNK and ERK pathways. In our study, one mechanism of angelicin‐mediated TRAIL sensitization is down‐regulation of c‐FLIP expression.…”

Section: Discussionmentioning

confidence: 95%

“…Angelicin can induce apoptosis in neuroblastoma cells via the intrinsic caspase‐mediated pathway and modulation of apoptosis‐related genes (Rahman, Kim, Yang, & Huh, ). Angelicin suppresses proliferation of human lung carcinoma cells by promoting G2/M arrest and induction of apoptosis (Li et al, ). However, whether angelicin has sensitizing effects against TRAIL‐mediated apoptotic cell death is unknown.…”

Section: Introductionmentioning

confidence: 99%

Angelicin potentiates TRAIL‐induced apoptosis in renal carcinoma Caki cells through activation of caspase 3 and down‐regulation of c‐FLIP expression

Min

Seo

et al. 2017

Drug Development Research

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Preclinical Research & Development Angelicin is a furocoumarin derived from Psoralea corylifolia L. fruit that has anti-inflammatory and anti-tumor activity. In the present study, the effect of angelicin in enhancing tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptotic cell death was studied in Caki (renal carcinoma) cells. Angelicin alone and TRAIL alone had no effect on apoptosis, but in combination these compounds markedly induced apoptosis in the cancer cell lines while not inducing apoptosis in normal cells. The combination treatment induced accumulation of the sub-G1 population, DNA fragmentation, and activated caspase 3 activity in Caki cells, induced down-regulation of c-FLIP expression post-translationally, and over-expression of c-FLIP markedly blocked apoptosis induced by combined treatment with angelicin plus TRAIL. This study provides evidence that angelicin might be a TRAIL sensitizer.

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“…Hence, the changes seen in the expression of apoptotic and anti-apoptotic proteins by angelicin is a positive indicator that angelicin has anticancer properties. Besides that, several different cells, such as promyelocytic leukaemia (HL-60), human lung cancer (A549), hepatoblastoma (HepG2), and hepatocellular carcinoma (Huh-7) cell lines, also yielded the same changes in the proteins mentioned above when incubated with angelicin for 24 or 48 h (Yuan et al, 2015;Li et al, 2016;Wang et al, 2017a). This shows that angelicin has the potential to be effective against multiple cancer cell lines.…”

Section: North America and Chinamentioning

confidence: 86%

Angelicin—A Furocoumarin Compound With Vast Biological Potential

et al. 2020

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Angelicin, a member of the furocoumarin group, is related to psoralen which is well known for its effectiveness in phototherapy. The furocoumarins as a group have been studied since the 1950s but only recently has angelicin begun to come into its own as the subject of several biological studies. Angelicin has demonstrated anti-cancer properties against multiple cell lines, exerting effects via both the intrinsic and extrinsic apoptotic pathways, and also demonstrated an ability to inhibit tubulin polymerization to a higher degree than psoralen. Besides that, angelicin too demonstrated anti-inflammatory activity in inflammatory-related respiratory and neurodegenerative ailments via the activation of NF-kB pathway. Angelicin also showed pro-osteogenesis and pro-chondrogenic effects on osteoblasts and pre-chondrocytes respectively. The elevated expression of proosteogenic and chondrogenic markers and activation of TGF-b/BMP, Wnt/b-catenin pathway confirms the positive effect of angelicin bone remodeling. Angelicin also increased the expression of estrogen receptor alpha (ERa) in osteogenesis. Other bioactivities, such as anti-viral and erythroid differentiating properties of angelicin, were also reported by several researchers with the latter even displaying an even greater aptitude as compared to the commonly prescribed drug, hydroxyurea, which is currently on the market. Apart from that, recently, a new application for angelicin against periodontitis had been studied, where reduction of bone loss was indirectly caused by its anti-microbial properties. All in all, angelicin appears to be a promising compound for further studies especially on its mechanism and application in therapies for a multitude of

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Angelicin inhibits human lung carcinoma A549 cell growth and migration through regulating JNK and ERK pathways

Cited by 28 publications

References 29 publications

Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness

Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness

Angelicin potentiates TRAIL‐induced apoptosis in renal carcinoma Caki cells through activation of caspase 3 and down‐regulation of c‐FLIP expression

Angelicin—A Furocoumarin Compound With Vast Biological Potential

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