gambogic acid/karcinóm prsníka

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Gambogic acid sensitizes breast cancer cells to TRAIL-induced apoptosis by promoting the crosstalk of extrinsic and intrinsic apoptotic signalings.

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Due to the ability of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) to induce cancer cell apoptosis selectively, TRAIL has attracted significant interest in the treatment of cancer. However, although TRAIL triggers apoptosis in a broad range of cancer cells, most primary

A novel redox/pH dual-responsive and hyaluronic acid-decorated multifunctional magnetic complex micelle for targeted gambogic acid delivery for the treatment of triple negative breast cancer.

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Gambogic acid (GA) is a naturally derived potent anticancer agent with extremely poor biocompatibility. In the present study, a novel of redox/pH dual-responsive multifunctional magnetic complex micelle (sPEG/HA/CSO-SS-Hex/Fe3O4/GA), which consisted of a reducible hexadecanol-modified chitosan

Gambogic acid-loaded pH-sensitive mixed micelles for overcoming breast cancer resistance.

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Multidrug resistance (MDR) is one of the major obstacles to the successful treatment of breast cancer. The overexpression of drug efflux transporters such as P-glycoprotein (P-gp) and of anti-apoptotic proteins like survivin are the major causes of MDR. Here, we developed a gambogic acid (GA)-loaded

Gambogic acid sensitizes resistant breast cancer cells to doxorubicin through inhibiting P-glycoprotein and suppressing survivin expression.

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The development of resistance to chemotherapeutic agents remains a major challenge to breast cancer chemotherapy. Overexpression of drug efflux transporters like P-glycoprotein (P-gp) and resistance to apoptosis are the two key factors that confer cancer drug resistance. Gambogic acid (GA), a major

Tumor neovasculature-targeted cationic PEGylated liposomes of gambogic acid for the treatment of triple-negative breast cancer.

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Gambogic acid (GA) is a naturally derived potent anticancer agent with extremely poor aqueous solubility. In the present study, positively charged PEGylated liposomal formulation of GA (GAL) was developed for parenteral delivery for the treatment of triple-negative breast cancer (TNBC). The GAL was

CD44 targeted redox-triggered self-assembly with magnetic enhanced EPR effects for effective amplification of gambogic acid to treat triple-negative breast cancer.

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Gambogic acid (GA) is a natural anti-tumor drug whose application is restricted by its poor aqueous solubility and inefficient bioavailability. Developing nanomaterials with excellent biocompatibility can amplify the therapeutic effects of GA. In this study, a tumor-targeted redox controllable

Gambogic acid increases the sensitivity to paclitaxel in drug‑resistant triple‑negative breast cancer via the SHH signaling pathway.

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Paclitaxel is the most frequently used therapy regimen for triple‑negative breast cancer (TNBC). However, chemoresistance frequently occurs, leading to enhanced failure rates of chemotherapy in TNBC; therefore, novel biological therapies are urgently needed. Gambogic acid (GA) has potent anticancer

Nanoparticles with Optimal Ratiometric Co-Delivery of Docetaxel with Gambogic Acid for Treatment of Multidrug-Resistant Breast Cancer.

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It has been reported that gambogic acid (GA), the main active component of gamboge, could directly inhibit and reduce the expression level of P-gp by promoting protein degradation through post-translational proteasome pathway. In this study, the optimal molar ratio of GA/docetaxel (DTX) that could

Gambogic Acid-Loaded Polymeric Micelles for Improved Therapeutic Effect in Breast Cancer.

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Gambogic acid (GA) possesses good anti-tumor efficacy in preclinical studies, however, its poor hydrophilicity, short blood circulation time and side effect limited its clinical application. In this work, monomethyl poly(ethylene glycol)-poly(ε-caprolactone) (MPEG-PCL) copolymer was synthesized and

Co-delivery of gambogic acid and TRAIL plasmid by hyaluronic acid grafted PEI-PLGA nanoparticles for the treatment of triple negative breast cancer.

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-based combination therapy and gene therapy are new strategies to potentially overcome the limitations of TRAIL, however, the lack of efficient and low toxic vectors remains the major obstacle. In this study, we developed a hyaluronic

Dimeric c(RGD) peptide conjugated nanostructured lipid carriers for efficient delivery of Gambogic acid to breast cancer.

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Background and purpose: Gambogic acid (GA) is a natural compound that exhibited a promising multi-target antitumor activity against several types of cancer. However, the clinical application of this drug is limited due to its poor solubility and low tumor cell-specific delivery. In this

Gambogic Acid lysinate induces apoptosis in breast cancer mcf-7 cells by increasing reactive oxygen species.

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Gambogic acid (GA) inhibits the proliferation of various human cancer cells. However, because of its water insolubility, the antitumor efficacy of GA is limited. Objectives. To investigate the antitumor activity of gambogic acid lysinate (GAL) and its mechanism. Methods. Inhibition of cell

Synthesis, structure-activity relationship and in vitro pharmacodynamics of A-ring modified caged xanthones in a preclinical model of inflammatory breast cancer.

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Inflammatory breast cancer (IBC) is a highly metastatic, lethal form of breast cancer that lacks targeted therapeutic strategies. Inspired by the promising cytotoxicity of gambogic acid and related caged xanthones in spheroids^MARY-X, an in vitro preclinical IBC model, we constructed a

Gambogic acid reduced bcl-2 expression via p53 in human breast MCF-7 cancer cells.

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OBJECTIVE In this study, we investigated the correlation between p53 and bcl-2 in gambogic acid (GA)-induced apoptosis. METHODS MTT assay was employed to evaluate MCF-7 cell viability after GA treatment. Cell morphological changes were observed follow-up under the inverted microscope after GA

Gambogic acid promotes apoptosis and resistance to metastatic potential in MDA-MB-231 human breast carcinoma cells.

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Gambogic acid (GA) is considered a potent anti-tumor agent for its multiple effects on cancer cells in vitro and in vivo. Low concentrations of GA (0.3-1.2 µmol/L) can suppress invasion of human breast carcinoma cells without affecting cell viability. To get a whole profile of the inhibition on

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