Acetyl-11-Keto-β-Boswellic Acid Inhibits Prostate Tumor Growth by Suppressing Vascular Endothelial Growth Factor Receptor 2–Mediated Angiogenesis

Pang, Xiufeng; Yi, Zhengfang; Zhang, Xiaoli; Sung, Bokyung; Qu, Wei; Lian, Xiao-Yuan; Aggarwal, Bharat B.; Liu, Mingyao

doi:10.1158/0008-5472.can-09-0755

Cited by 198 publications

(151 citation statements)

References 37 publications

(41 reference statements)

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“…Our present investigation showed that both mRNA and protein expression of VEGF were dose-dependently suppressed by nitidine chloride via STAT3 inhibition in human gastric cancer cells. VEGF was initially thought to mediate its signaling in a paracrine manner by acting on neighboring endothelial cells via VEGFR2, which was specifically expressed on the endothelial cell surface and believed to regulate the majority of the angiogenic effects of VEGF (23,36,41). In this study, we found that nitidine chloride dose-dependently inhibited the phosphorylation of VEGFR2 (Tyr 1,175 ) in HUVECs, which may lead to the inhibition of a number of downstream signaling cascades.…”

Section: Discussionmentioning

confidence: 62%

“…Formation of tubular structures of endothelial cell was studied in vitro as previously described (23). HUVECs were pretreated with nitidine chloride (5 and 10 mmol/L) for 1 hour and then seeded onto the Matrigel layer in 48-well plates at a density of 5 Â 10 4 to 1 Â 10 5 cells per well.…”

Section: Endothelial Cell Capillary-like Tube Formation Assaymentioning

confidence: 99%

“…Nitidine chloride-mediated cell apoptosis was assayed by Annexin V-fluorescein isothiocyanate (FITC) and propidium iodide staining (ApopNexin Annexin V FITC apoptosis kit; Millipore) as described earlier (23).…”

Section: Annexin V/propidium Iodide Staining Assaymentioning

confidence: 99%

“…It has been known that VEGF signaling events relevant to tumor angiogenesis are mainly mediated by VEGF receptor 2 (VEGFR2) phosphorylation (23). Therefore, we first tested the action of nitidine chloride on this critical receptor tyrosine kinase on endothelial cell membrane.…”

Section: Nitidine Chloride Blocks Vegf-induced Stat3 Activation In Enmentioning

confidence: 99%

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Inhibition of STAT3 Signaling Pathway by Nitidine Chloride Suppressed the Angiogenesis and Growth of Human Gastric Cancer

Chen

Wang

Lin

et al. 2012

Molecular Cancer Therapeutics

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137

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STAT3 has been strongly implicated in human malignancies, and constitutive activation of STAT3 serves a crucial role in cell survival, angiogenesis, immune evasion, and inflammation. In this study, we showed that nitidine chloride, a natural phytochemical alkaloid derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through STAT3 signaling cascade. Nitidine chloride dose dependently suppressed VEGFinduced endothelial cell proliferation, migration, and tubular structure formation in vitro and dramatically reduced VEGF-triggered neovascularization in mouse cornea and Matrigel plugs in vivo. This angiogenesis inhibition mediated by nitidine chloride was well interpreted by the suppression of Janus kinase 2/STAT3 signaling and STAT3 DNA-binding activity in endothelial cells. Furthermore, nitidine chloride suppressed the constitutively activated STAT3 protein, its DNA-binding activity, and the expression of STAT3-dependent target genes, including cyclin D1, Bcl-xL, and VEGF in human gastric cancer cells. Consistent with the earlier findings, nitidine chloride inhibited gastric tumor cell growth and induced tumor cell apoptosis in vitro and effectively suppressed the volume, weight, and microvessel density of human SGC-7901 gastric solid tumors (n ¼ 8) at a dosage of 7 mg/kg/d (intraperitoneal injection). Immunohistochemistry and Western blot analysis further revealed that the expression of STAT3, CD31, and VEGF protein in xenografts was remarkably decreased by the alkaloid. Taken together, we propose that nitidine chloride is a promising anticancer drug candidate as a potent STAT3 signaling inhibitor. Mol Cancer Ther; 11(2); 277-87. Ó2011 AACR.

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Section: Discussionmentioning

confidence: 62%

Section: Endothelial Cell Capillary-like Tube Formation Assaymentioning

confidence: 99%

Section: Annexin V/propidium Iodide Staining Assaymentioning

confidence: 99%

Section: Nitidine Chloride Blocks Vegf-induced Stat3 Activation In Enmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of STAT3 Signaling Pathway by Nitidine Chloride Suppressed the Angiogenesis and Growth of Human Gastric Cancer

Chen

Wang

Lin

et al. 2012

Molecular Cancer Therapeutics

Self Cite

137

122

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“…They found that the oral administration of AKBA (50-200 mg/kg) dose-dependently inhibited the growth of colorectal tumors with no adverse side effects. Other studies showed that BA and its novel cyano derivative of 11-keto-b-boswellic acid inhibited Ehrlich ascites tumor [73,74], novel 11-keto-b-boswellic acid inhibited promyelocytic leukemia cells, HL-60, in both ascites and solid tumor model, was mediated through the inhibition of topoisomerase I and II [75] and AKBA suppressed human prostate tumor xenografts in nude mice [76]. Shah et al showed that 24-NH2 substituted b-boswellic acid derivatives exhibited much more potent apoptosis induction and cell proliferation inhibition than their parent 24-COOH compounds.…”

Section: Boswellic Acidmentioning

confidence: 98%

Targeted inhibition of tumor proliferation, survival, and metastasis by pentacyclic triterpenoids: Potential role in prevention and therapy of cancer

et al. 2012

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a b s t r a c tOver the last two decades, extensive research on plant-based medicinal compounds has revealed exciting and important pharmacological properties and activities of triterpenoids. Fruits, vegetables, cereals, pulses, herbs and medicinal plants are all considered to be biological sources of these triterpenoids, which have attracted great attention especially for their potent anti-inflammatory and anti-cancer activities. Published reports in the past have described the molecular mechanism(s) underlying the various biological activities of triterpenoids which range from inhibition of acute and chronic inflammation, inhibition of tumor cell proliferation, induction of apoptosis, suppression of angiogenesis and metastasis. However systematic analysis of various pharmacological properties of these important classes of compounds has not been done. In this review, we describe in detail the pre-clinical chemopreventive and therapeutic properties of selected triterpenoids that inhibit multiple intracellular signaling molecules and transcription factors involved in the initiation, progression and promotion of various cancers. Molecular targets modulated by these triterpenoids comprise, cytokines, chemokines, reactive oxygen intermediates, oncogenes, inflammatory enzymes such as COX-2, 5-LOX and MMPs, anti-apoptotic proteins, transcription factors such as NF-jB, STAT3, AP-1, CREB, and Nrf2 (nuclear factor erythroid 2-related factor) that regulate tumor cell proliferation, transformation, survival, invasion, angiogenesis, metastasis, chemoresistance and radioresistance. Finally, this review also analyzes the potential role of novel synthetic triterpenoids identified recently which mimic natural triterpenoids in physical and chemical properties and are moving rapidly from bench to bedside research.

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Evaluation of anticancer effects of frankincense on breast cancer stem‐like cells

et al. 2022

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Background: Relapse and metastasis in breast cancer are linked to cancer stem cells (CSCs) resistant to anticancer therapies. The presence of cancer stem-like cells (CSLCs) and their ability to self-renew is determined by in vitro spheroid formation.Aims: Many studies have found that frankincense has anticancer impacts, although these effects on breast CSLCs have never been evaluated. Methods and results:A population of heterogeneous breast tumor cells was extracted from the tumor mass after generating an animal model of triple-negative breast cancer (TNBC). Spheroid formation was used as an in vitro assay to determine the existence of CSLCs in these cells. MTT assay was used to determine frankincense's cytotoxic activity.An annexin V-propidium iodide (PI) staining and scratch test were used to assess the induction of apoptosis and antimetastatic effects of frankincense. The frankincense extract has significant cytotoxic and apoptotic effects on breast CSLCs. Although, the breast CSLCs are more resistant to these impacts than other breast cancer cells. Conclusion:Our study is the first report that indicates that frankincense extract has anticancer properties in breast CSLCs. Compared to many anticancer chemicals, which have limited potential to battle cancer stem cells, frankincense is an appropriate option to combat breast CSCs.

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Acetyl-11-Keto-β-Boswellic Acid Inhibits Prostate Tumor Growth by Suppressing Vascular Endothelial Growth Factor Receptor 2–Mediated Angiogenesis

Cited by 198 publications

References 37 publications

Inhibition of STAT3 Signaling Pathway by Nitidine Chloride Suppressed the Angiogenesis and Growth of Human Gastric Cancer

Inhibition of STAT3 Signaling Pathway by Nitidine Chloride Suppressed the Angiogenesis and Growth of Human Gastric Cancer

Targeted inhibition of tumor proliferation, survival, and metastasis by pentacyclic triterpenoids: Potential role in prevention and therapy of cancer

Evaluation of anticancer effects of frankincense on breast cancer stem‐like cells

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