Herbal Extract SH003 Suppresses Tumor Growth and Metastasis of MDA-MB-231 Breast Cancer Cells by Inhibiting STAT3-IL-6 Signaling

Choi, Youn Kyung; Cho, Sung Gook; Woo, Sang‐Mi; Yun, Yee Jin; Park, Sunju; Shin, Yong Cheol; Ko, Seong‐Gyu

doi:10.1155/2014/492173

Cited by 50 publications

(75 citation statements)

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“…Moreover, SH003 inhibited the interaction between VEGF and VEGFR1, while the inhibitions showed different IC 50 values (Figure 5B). We recently confirmed that SH003 and its herbal components contained cucurbitacin D, decursin, formononetin, and nodakenin [13]. Therefore, we further examined whether those chemical compounds inhibits VEGF binding to VEGFR2.…”

Section: Resultsmentioning

confidence: 93%

“…Our previous study showed that SH003 at higher concentrations caused breast cancer cell death by inhibiting STAT3-mediated signaling pathway [13]. SH003 concentrations tested in this study was lowered than those in the previous study [13], as we considered the metronomic approach to target tumor angiogenesis [48–50].…”

Section: Discussionmentioning

confidence: 99%

“…SH003 concentrations tested in this study was lowered than those in the previous study [13], as we considered the metronomic approach to target tumor angiogenesis [48–50]. SH003 significantly inhibited VEGF-induced angiogenic processes in vitro including endothelial cell migration, invasion and capillary-like structure formation with no effect on the proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous study found that SH003 reduced CD31-stained vessel numbers in tumor tissues [13], which raised a question of whether SH003 directly affects tumor angiogenesis. Ag inhibits VEGF-induced angiogenesis, while Am induces angiogenesis [18, 34–36].…”

Section: Introductionmentioning

confidence: 99%

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SH003 represses tumor angiogenesis by blocking VEGF binding to VEGFR2

et al. 2016

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Tumor angiogenesis is a key feature of cancer progression, because a tumor requires abundant oxygen and nutrition to grow. Here, we demonstrate that SH003, a mixed herbal extract containing Astragalus membranaceus (Am), Angelica gigas (Ag) and Trichosanthes Kirilowii Maximowicz (Tk), represses VEGF-induced tumor angiogenesis both in vitro and in vivo. SH003 inhibited VEGF-induced migration, invasion and tube formation in human umbilical vein endothelial cells (HUVEC) with no effect on the proliferation. SH003 reduced CD31-positive vessel numbers in tumor tissues and retarded tumor growth in our xenograft mouse tumor model, while SH003 did not affect pancreatic tumor cell viability. Consistently, SH003 inhibited VEGF-stimulated vascular permeability in ears and back skins. Moreover, SH003 inhibited VEGF-induced VEGFR2-dependent signaling by blocking VEGF binding to VEGFR2. Therefore, our data conclude that SH003 represses tumor angiogenesis by inhibiting VEGF-induced VEGFR2 activation, and suggest that SH003 may be useful for treating cancer.

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Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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SH003 represses tumor angiogenesis by blocking VEGF binding to VEGFR2

et al. 2016

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“…Recent data have demonstrated that IL-6 induced MDA-MB-231 cell invasion via the STAT-3 signaling pathway. 40) Moreover, inhibition of IL-6 signaling has been shown to attenuate tumor growth and angiogenesis and metastatic events in breast cancer patients.…”

Section: Discussionmentioning

confidence: 99%

Proanthocyanidin in Red Rice Inhibits MDA-MB-231 Breast Cancer Cell Invasion <i>via</i> the Expression Control of Invasive Proteins

Pintha

Yodkeeree

Limtrakul

2015

Biological & Pharmaceutical Bulletin

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Proanthocyanidin is one of the main active compounds found in red jasmine rice. We previously reported that red rice extract could reduce cancer cell invasion. However, the direct effect of proanthocyanidin from red rice on the invasion of cancer cells and the exact molecular mechanism remained unclear. Here, we report for the first time that proanthocyanidin-rich fraction from red rice (PRFR) reduced the migration and invasion of MDA-MB-231 human breast cancer cells. The types of proanthocyanidin in PRFR were identified as procyanidins and prodelphinidins by acid hydrolysis. For cancer cell invasion, degradation of the extracellular matrix (ECM) is required. Treatment of the cells with PRFR reduced the expression of ECM degradation-associated proteins, including matrix metalloproteinase-9 (MMP-9), membrane type-1 matrix metalloproteinase, urokinase plasminogen activator, urokinase plasminogen activator receptor and plasminogen activator-1. Moreover, PRFR also reduced the activity of collagenase and MMP-9. Furthermore, PRFR significantly suppressed the expression of intercellular adhesion molecule-1 and interleukin-6. We also found that PRFR reduced the DNA-binding activity of nuclear factor kappa B (NF-κB), which is the expressed mediator of ECM degradation-associated proteins. These results suggest that proanthocyanidin from red rice mediates MDA-MB-231 breast cancer cell invasion by altering the expression of the invasion-associated proteins, possibly by targeting NF-κB activity.Key words proanthocyanidin; red rice; invasion; nuclear factor kappa B Breast cancer is a leading cause of mortality among women worldwide including in Thailand. The metastasis of breast cancer to other sites such as the liver, bones, the lungs and lymph nodes is a critical factor contributing to the increased rate of mortality in breast cancer patients.1) The metastasis of cancer cells is a complex process involving cell adhesion, migration and proteolytic degradation of the extracellular matrix (ECM). Degradation of ECM components is an important step in the metastatic process, and it is regulated by the activation of ECM degradation enzymes such as matrix metalloproteinases (MMPs) and urokinase plasminogen activator (uPA). 2)Several scientific studies have shown that uPA plays an important role in tumor metastasis and over-expression of uPA in breast cancer is a strong indicator of the poor prognosis.3)The uPA converts the inactive plasminogen into the active serine protease plasmin, which is involved in the degradation of ECM. The uPA system consists of uPA, the uPA receptor (uPAR), plasminogen and its inhibitor, plasminogen inhibitor types 1 and 2 (PAI-1 and -2). The binding of uPA to uPAR not only promotes cancer metastasis but also generates signal transduction that allows enhanced cell survival and migration. 3)MMPs essentially degrade all ECM components surrounding the cancer cells, allowing them to spread from the primary site. Up-regulation of several MMPs such as MMP-2, -3, -9 and membrane type-1 matrix metalloproteinases ...

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What Has Come out from Phytomedicines and Herbal Edibles for the Treatment of Cancer?

Bonam

Tunki

et al. 2018

ChemMedChem

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Several modern treatment strategies have been adopted to combat cancer with the aim of minimizing toxicity. Medicinal plant-based compounds with the potential to treat cancer have been widely studied in preclinical research and have elicited many innovations in cutting-edge clinical research. In parallel, researchers have eagerly tried to decrease the toxicity of current chemotherapeutic agents either by combining them with herbals or in using herbals alone. The aim of this article is to present an update of medicinal plants and their bioactive compounds, or mere changes in the bioactive compounds, along with herbal edibles, which display efficacy against diverse cancer cells and in anticancer therapy. It describes the basic mechanism(s) of action of phytochemicals used either alone or in combination therapy with other phytochemicals or herbal edibles. This review also highlights the remarkable synergistic effects that arise between certain herbals and chemotherapeutic agents used in oncology. The anticancer phytochemicals used in clinical research are also described; furthermore, we discuss our own experience related to semisynthetic derivatives, which are developed based on phytochemicals. Overall, this compilation is intended to facilitate research and development projects on phytopharmaceuticals for successful anticancer drug discovery.

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Herbal Extract SH003 Suppresses Tumor Growth and Metastasis of MDA-MB-231 Breast Cancer Cells by Inhibiting STAT3-IL-6 Signaling

Cited by 50 publications

References 44 publications

SH003 represses tumor angiogenesis by blocking VEGF binding to VEGFR2

SH003 represses tumor angiogenesis by blocking VEGF binding to VEGFR2

Proanthocyanidin in Red Rice Inhibits MDA-MB-231 Breast Cancer Cell Invasion <i>via</i> the Expression Control of Invasive Proteins

What Has Come out from Phytomedicines and Herbal Edibles for the Treatment of Cancer?

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