Artemisinin derivative FO-ARS-123 as a novel VEGFR2 inhibitor suppresses angiogenesis, cell migration, and invasion

Lu, Xiaohua; Elbadawi, Mohamed; Blatt, Sebastian; Saeed, Mohamed E.M.; Xiao, Xiaolin; Ma, Xiaohua; Fleischer, Edmond; Kämmerer, Peer W.; Efferth, Thomas

doi:10.1016/j.cbi.2022.110062

Cited by 5 publications

(2 citation statements)

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“…17 The vascular endothelial growth factor (VEGF), which is overexpressed in the endothelium of multiple types of solid tumors, plays critical roles in tumor angiogenesis and metastatic spread. 18 Therefore, VEGF is a predominant target for the development of antiangiogenesis agents. 19 Cyclooxygenase-2 (COX-2), an inflammatory mediator, is overexpressed in premalignant and malignant tumor cells; thus, it plays an important role in breast cancer proliferation, angiogenesis, and metastasis.…”

Section: ■ Introductionmentioning

confidence: 99%

“…On the other hand, checkpoint blockade therapy can reprogram the tumor immune microenvironment and facilitate vessel normalization . The vascular endothelial growth factor (VEGF), which is overexpressed in the endothelium of multiple types of solid tumors, plays critical roles in tumor angiogenesis and metastatic spread . Therefore, VEGF is a predominant target for the development of antiangiogenesis agents .…”

Section: Introductionmentioning

confidence: 99%

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Combination Nano-Delivery Systems Remodel the Immunosuppressive Tumor Microenvironment for Metastatic Triple-Negative Breast Cancer Therapy

Bai,

Liu,

You

et al. 2024

Mol. Pharmaceutics

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Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer for which effective therapies are lacking. Targeted remodeling of the immunosuppressive tumor microenvironment (TME) and activation of the body’s immune system to fight tumors with well-designed nanoparticles have emerged as pivotal breakthroughs in tumor treatment. To simultaneously remodel the immunosuppressive TME and trigger immune responses, we designed two potential therapeutic nanodelivery systems to inhibit TNBC. First, the bromodomain-containing protein 4 (BRD4) inhibitor JQ1 and the cyclooxygenase-2 (COX-2) inhibitor celecoxib (CXB) were coloaded into chondroitin sulfate (CS) to obtain CS@JQ1/CXB nanoparticles (NPs). Then, the biomimetic nanosystem MM@P3 was prepared by coating branched polymer poly(β-amino ester) self-assembled NPs with melittin embedded macrophage membranes (MM). Both in vitro and in vivo, the CS@JQ1/CXB and MM@P3 NPs showed excellent immune activation efficiencies. Combination treatment exhibited synergistic cytotoxicity, antimigration ability, and apoptosis-inducing and immune activation effects on TNBC cells and effectively suppressed tumor growth and metastasis in TNBC tumor-bearing mice by activating the tumor immune response and inhibiting angiogenesis. In summary, this study offers a novel combinatorial immunotherapeutic strategy for the clinical TNBC treatment.

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Section: ■ Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%