Combination of targeted daunorubicin liposomes and targeted emodin liposomes for treatment of invasive breast cancer

Fu, Min; Tang, Wei; Liu, Jingjing; Gong, Xiaoqing; Kong, Liang; Yao, Xuemin; Jing, Ming; Cai, Fu-Yi; Li, Xuetao; Ju, Rui-Jun

doi:10.1080/1061186x.2019.1656725

Cited by 46 publications

(30 citation statements)

References 40 publications

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“…Cells treated with the newly-developed, liposomal-based, theranostic system exhibited significantly reduced oncogenic microRNA, mRNA, and colony formation, while tumor suppression was meaningfully increased in the treated group. Similarly, a new type of Arginine 8 -Glycine-Aspartic acid-modified, specific liposomal system was engineered for the separate encapsulation of emodin and daunorubicin [ 292 ]. The two-targeted liposomes were then combined to prevent tumor metastasis and disrupt vasculogenic mimicry channels.…”

Section: Stimuli-responsive Polymeric Nanocarriers For Theranosismentioning

confidence: 99%

“…Insight into the mechanism suggests the downregulation of some metastasis-associated proteins, including VE-cad, HIF-1α, TGF-β1, and MMP-2 by the action of Arginine 8 -Glycine-Aspartic acid-modified daunorubicin and emodin liposomes. The specifically modified liposomes also facilitated the selective accumulation of chemotherapeutic drugs at the tumor site to exhibit direct antitumor activities, consequently providing a promising theranostic system for breast cancer [ 292 ].…”

Section: Stimuli-responsive Polymeric Nanocarriers For Theranosismentioning

confidence: 99%

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Stimuli-Responsive Polymeric Nanocarriers for Drug Delivery, Imaging, and Theragnosis

et al. 2020

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In the past few decades, polymeric nanocarriers have been recognized as promising tools and have gained attention from researchers for their potential to efficiently deliver bioactive compounds, including drugs, proteins, genes, nucleic acids, etc., in pharmaceutical and biomedical applications. Remarkably, these polymeric nanocarriers could be further modified as stimuli-responsive systems based on the mechanism of triggered release, i.e., response to a specific stimulus, either endogenous (pH, enzymes, temperature, redox values, hypoxia, glucose levels) or exogenous (light, magnetism, ultrasound, electrical pulses) for the effective biodistribution and controlled release of drugs or genes at specific sites. Various nanoparticles (NPs) have been functionalized and used as templates for imaging systems in the form of metallic NPs, dendrimers, polymeric NPs, quantum dots, and liposomes. The use of polymeric nanocarriers for imaging and to deliver active compounds has attracted considerable interest in various cancer therapy fields. So-called smart nanopolymer systems are built to respond to certain stimuli such as temperature, pH, light intensity and wavelength, and electrical, magnetic and ultrasonic fields. Many imaging techniques have been explored including optical imaging, magnetic resonance imaging (MRI), nuclear imaging, ultrasound, photoacoustic imaging (PAI), single photon emission computed tomography (SPECT), and positron emission tomography (PET). This review reports on the most recent developments in imaging methods by analyzing examples of smart nanopolymers that can be imaged using one or more imaging techniques. Unique features, including nontoxicity, water solubility, biocompatibility, and the presence of multiple functional groups, designate polymeric nanocues as attractive nanomedicine candidates. In this context, we summarize various classes of multifunctional, polymeric, nano-sized formulations such as liposomes, micelles, nanogels, and dendrimers.

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Section: Stimuli-responsive Polymeric Nanocarriers For Theranosismentioning

confidence: 99%

Section: Stimuli-responsive Polymeric Nanocarriers For Theranosismentioning

confidence: 99%

Stimuli-Responsive Polymeric Nanocarriers for Drug Delivery, Imaging, and Theragnosis

et al. 2020

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“…Destruction of VM channels and inhibition of tumor metastasis of liposomes were evaluated on MDA-MB-435S cells in vivo and in vitro by Fu et al When we evaluate in vitro andin vivo studies together, targeted liposomes loaded with daunorubicin and emodin were accumulated in the tumor area with the effect of enhanced permeability and retention (EPR). An increased absorption was also observed, modification of the surface of liposomes was also improved cellular uptake and targeting and the formation of VM channels and metastasis are inhibited [ 197 ]. It has been stated that the combination of liposomes can be used as an effective treatment method with the synergistic effect of daunorubicin with antitumor effect and emodin, which has been proven effective against cancer by many studies.…”

Section: Nano-drug Delivery Strategies For Emodinmentioning

confidence: 99%

Is Emodin with Anticancer Effects Completely Innocent? Two Sides of the Coin

Akkol

Tatlı

Karatoprak

et al. 2021

Cancers

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Many anticancer active compounds are known to have the capacity to destroy pathologically proliferating cancer cells in the body, as well as to destroy rapidly proliferating normal cells. Despite remarkable advances in cancer research over the past few decades, the inclusion of natural compounds in researches as potential drug candidates is becoming increasingly important. However, the perception that the natural is reliable is an issue that needs to be clarified. Among the various chemical classes of natural products, anthraquinones have many biological activities and have also been proven to exhibit a unique anticancer activity. Emodin, an anthraquinone derivative, is a natural compound found in the roots and rhizomes of many plants. The anticancer property of emodin, a broad-spectrum inhibitory agent of cancer cells, has been detailed in many biological pathways. In cancer cells, these molecular mechanisms consist of suppressing cell growth and proliferation through the attenuation of oncogenic growth signaling, such as protein kinase B (AKT), mitogen-activated protein kinase (MAPK), HER-2 tyrosine kinase, Wnt/-catenin, and phosphatidylinositol 3-kinase (PI3K). However, it is known that emodin, which shows toxicity to cancer cells, may cause kidney toxicity, hepatotoxicity, and reproductive toxicity especially at high doses and long-term use. At the same time, studies of emodin, which has poor oral bioavailability, to transform this disadvantage into an advantage with nano-carrier systems reveal that natural compounds are not always directly usable compounds. Consequently, this review aimed to shed light on the anti-proliferative and anti-carcinogenic properties of emodin, as well as its potential toxicities and the advantages of drug delivery systems on bioavailability.

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“…Emodin displays a variety of pharmacological and biological functions, including some anti-inflammatory, antibacterial and chemoprophylactic effects (9)(10)(11). In addition, previous studies have demonstrated that emodin exhibits some anticancer effects in breast, pancreatic and cervical cancers by inhibiting cancer cell proliferation and increasing cancer cell apoptosis and chemosensitization (12)(13)(14). Other studies have reported that emodin can reverse the chemoresistance in certain types of cancer, including leukemia, NSCLC and gallbladder cancer (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Emodin enhances cisplatin sensitivity in non-small cell lung cancer through Pgp downregulation

Peng

Wang

et al. 2021

Oncol Lett

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Cisplatin resistance is one of the main causes of chemotherapy failure and tumor progression in non-small cell lung cancer (NSCLC). Emodin has been demonstrated to induce NSCLC cell apoptosis and act as a potential cancer therapeutic agent. However, whether emodin could affect NSCLC cell sensitivity toward cisplatin remains unclear. The present study aimed to determine the effect of emodin and cisplatin combination on the chemosensitivity of NSCLC cells. A549 and H460 cells were treated with different concentrations of cisplatin and/or emodin. Cell Counting Kit-8, fluorescence microscopy, immunofluorescence assays and flow cytometry were used to determine cell proliferation, drug efflux, DNA damage level and cell apoptosis, respectively. P-glycoprotein (Pgp) and multidrug resistance-associated protein 1 (MRP1) expression was detected by western blotting. The results demonstrated that emodin and cisplatin inhibited the proliferation of A549 and H460 cells. Furthermore, emodin inhibited the drug efflux in A549 and H460 cells in a dose-dependent manner. In addition, emodin enhanced cisplatin-induced apoptosis and DNA damage in A549 and H460 cells. Emodin also decreased Pgp expression in A549 and H460 cells in a dose-dependent manner; however, it had no effect on MRP1 expression. Taken together, the results from the present study demonstrated that emodin can increase A549 and H460 cell sensitivity to cisplatin by inhibiting Pgp expression. Emodin may therefore be considered as an effective adjuvant for cisplatin treatment.

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Combination of targeted daunorubicin liposomes and targeted emodin liposomes for treatment of invasive breast cancer

Cited by 46 publications

References 40 publications

Stimuli-Responsive Polymeric Nanocarriers for Drug Delivery, Imaging, and Theragnosis

Stimuli-Responsive Polymeric Nanocarriers for Drug Delivery, Imaging, and Theragnosis

Is Emodin with Anticancer Effects Completely Innocent? Two Sides of the Coin

Emodin enhances cisplatin sensitivity in non-small cell lung cancer through Pgp downregulation

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