A novel double-targeted nondrug delivery system for targeting cancer stem cells

Qiao, Shupei; Zhao, Yufang; Geng, Shuai; Li, Yong; Hou, Xiaolu; Liu, Yi; Lin, Feng-Huei; Yao, Lifen; Tian, Weiming

doi:10.2147/ijn.s116230

Cited by 34 publications

(19 citation statements)

References 51 publications

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“…The enrichment of the CSC population may cause drug resistance, leading to recurrence and metastasis of tumors with poor prognosis (4,10,11,12,15,(21)(22)(23)25,28,36,39). In the present study, MDA-MB-468-Dox and 4T1-Dox cells were used to investigate whether Dox induced CSC-enrichment.…”

Section: Discussionmentioning

confidence: 97%

“…Drug resistance was originally attributed to drug efflux mediated by adenosine triphosphate-binding cassette transporter (8,9). Increasing evidence has indicated the existence of cancer stem cells (CSCs) in breast cancer, and these CSCs are involved in the process of cancer initiation, metastasis, recurrence and therapeutic resistance (3,6,(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22). CSCs have cancer-initiating capability and metastatic potential (4,(23)(24)(25)(26)(27).…”

Section: Introductionmentioning

confidence: 99%

“…CD44 is a cell surface receptor for the extracellular matrix protein hyaluronan. CSCs expressing CD44 are considered to be responsible for adhesion, invasion, metastasis and the acquisition of resistance to apoptosis (6,12,25,(28)(29)(30)(31)(32)(33). ATP-binding cassette subfamily G member 2 (ABCG2) is overexpressed in several types of tumor and tumor cell lines (5,10,17,(34)(35)(36)(37)(38).…”

Section: Introductionmentioning

confidence: 99%

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Stat3/Oct-4/c-Myc signal circuit for regulating stemness-mediated doxorubicin resistance of triple-negative breast cancer cells and inhibitory effects of WP1066

et al. 2018

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Doxorubicin (Dox) is widely used in the treatment of triple-negative breast cancer cells (TNBCs), however resistance limits its effectiveness. Cancer stem cells (CSCs) are associated with Dox resistance in MCF-7 estrogen receptor positive breast cancer cells. Signal transducer and activator of transcription 3 (Stat3) may functionally shift non-CSCs towards CSCs. However, whether Stat3 drives the formation of CSCs during the development of resistance in TNBC, and whether a Stat3 inhibitor reverses CSC-mediated Dox resistance, remains to be elucidated. In the present study, human MDA-MB-468 and murine 4T1 mammary carcinoma cell lines with the typical characteristics of TNBCs, were compared with estrogen receptor-positive MCF-7 cells as a model system. The MTT assay was used to detect cytotoxicity of Dox. In addition, the expression levels of CSC-specific markers and transcriptional factors were measured by western blotting, immunofluorescence staining and flow cytometry. The mammosphere formation assay was used to detect stem cell activity. Under long-term continuous treatment with Dox at a low concentration, TNBC cultures not only exhibited a drug-resistant phenotype, but also showed CSC properties. These Dox-resistant TNBC cells showed activation of Stat3 and high expression levels of pluripotency transcription factors octamer-binding transcription factor-4 (Oct-4) and c-Myc, which was different from the high expression of superoxide dismutase 2 (Sox2) in Dox-resistant MCF-7 cells. WP1066 inhibited the phosphorylation of Stat3, and decreased the expression of Oct-4 and c-Myc, leading to a reduction in the CD44-positive cell population, and restoring the sensitivity of the cells to Dox. Taken together, a novel signal circuit of Stat3/Oct-4/c-Myc was identified for regulating stemness-mediated Dox resistance in TNBC. The Stat3 inhibitor WP1066 was able to overcome the resistance to Dox through decreasing the enrichment of CSCs, highlighting the therapeutic potential of WP1066 as a novel sensitizer of Dox-resistant TNBC.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Stat3/Oct-4/c-Myc signal circuit for regulating stemness-mediated doxorubicin resistance of triple-negative breast cancer cells and inhibitory effects of WP1066

et al. 2018

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“…41 PLGA is a potential vehicle candidate for the sustained release of proteins that show promise as treatments for cardiac diseases. [42][43][44][45] Moreover, PEG is effective in preventing NP phagocytosis by …”

Section: Discussionmentioning

confidence: 99%

Spatiotemporal delivery of nanoformulated liraglutide for cardiac regeneration after myocardial infarction

Qi¹,

Lü

Li³

et al. 2017

IJN

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The local, intramyocardial injection of proteins into the infarcted heart is an attractive option to initiate cardiac regeneration after myocardial infarction (MI). Liraglutide, which was developed as a treatment for type 2 diabetes, has been implicated as one of the most promising protein candidates in cardiac regeneration. A significant challenge to the therapeutic use of this protein is its short half-life in vivo. In this study, we evaluated the therapeutic effects and long-term retention of liraglutide loaded in poly(lactic- co -glycolic acid)–poly(ethylene glycol) (PLGA–PEG) nanoparticles (NP-liraglutide) on experimental MI. PLGA–PEG nanoparticles (NPs) have been shown to efficiently load liraglutide and release bioactive liraglutide in a sustained manner. For in vitro test, the released liraglutide retained bioactivity, as measured by its ability to activate liraglutide signaling pathways. Next, we compared the effects of an intramyocardial injection of saline, empty NPs, free liraglutide and NP-liraglutide in a rat model of MI. NPs were detected in the myocardium for up to 4 weeks. More importantly, an intramyocardial injection of NP-liraglutide was sufficient to improve cardiac function ( P <0.05), attenuate the infarct size ( P <0.05), preserve wall thickness ( P <0.05), promote angiogenesis ( P <0.05) and prevent cardiomyocyte apoptosis ( P <0.05) at 4 weeks after injection without affecting glucose levels. The local, controlled, intramyocardial delivery of NP-liraglutide represents an effective and promising strategy for the treatment of MI.

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“…Qiao et al showed that the hyaluronic acid and DCLK1 antibody dual-decorated nanoparticles target the mammospheres better than single-targeted system. 82 This may be an interesting strategy that could be investigated further.…”

Section: Nanotherapy Of Breast Cancer Stem Cells (Bcscs)mentioning

confidence: 99%

Nanomedicine applications in the treatment of breast cancer: current state of the art

Xue

et al. 2017

IJN

158

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Breast cancer is the most common malignant disease in women worldwide, but the current drug therapy is far from optimal as indicated by the high death rate of breast cancer patients. Nanomedicine is a promising alternative for breast cancer treatment. Nanomedicine products such as Doxil ® and Abraxane ® have already been extensively used for breast cancer adjuvant therapy with favorable clinical outcomes. However, these products were originally designed for generic anticancer purpose and not specifically for breast cancer treatment. With better understanding of the molecular biology of breast cancer, a number of novel promising nanotherapeutic strategies and devices have been developed in recent years. In this review, we will first give an overview of the current breast cancer treatment and the updated status of nanomedicine use in clinical setting, then discuss the latest important trends in designing breast cancer nanomedicine, including passive and active cancer cell targeting, breast cancer stem cell targeting, tumor microenvironment-based nanotherapy and combination nanotherapy of drug-resistant breast cancer. Researchers may get insight from these strategies to design and develop nanomedicine that is more tailored for breast cancer to achieve further improvements in cancer specificity, antitumorigenic effect, antimetastasis effect and drug resistance reversal effect.

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A novel double-targeted nondrug delivery system for targeting cancer stem cells

Cited by 34 publications

References 51 publications

Stat3/Oct-4/c-Myc signal circuit for regulating stemness-mediated doxorubicin resistance of triple-negative breast cancer cells and inhibitory effects of WP1066

Stat3/Oct-4/c-Myc signal circuit for regulating stemness-mediated doxorubicin resistance of triple-negative breast cancer cells and inhibitory effects of WP1066

Spatiotemporal delivery of nanoformulated liraglutide for cardiac regeneration after myocardial infarction

Nanomedicine applications in the treatment of breast cancer: current state of the art

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