Inorganic kernel - Supported asymmetric hybrid vesicles for targeting delivery of STAT3-decoy oligonucleotides to overcome anti-HER2 therapeutic resistance of BT474R

Shi, Kai; Fang, Yan; Gao, Shan; Yang, Dongjuan; Bi, Hongshu; Xue, Jianxiu; Lu, Anqi; Li, Yuai; Ke, Liyuan; Lin, Xiaojie; Jin, Xuechao; Li, Min

doi:10.1016/j.jconrel.2018.04.023

Cited by 17 publications

(14 citation statements)

References 58 publications

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“…Plasmid-based Stat3 siRNA introduced by CaCl 2 modified Hydroxyapatite (HAP) nanoparticles was able to lower the protein expression of Stat3 and p-Stat3 in prostate tumor bearing mice at the same time downregulated the expression of Stat3 -associated downstream genes (170). A hybrid of lipid and polymer vesicles with calcium phosphate as the solid kernel (CaP@HA) was used to introduce STAT3-specific decoy oligonucleotides (STAT3-decoy-ODNs) into TRAZ-resistant HER2-positive breast cancer cells (171). ODNs packaged with CaP@HA showed significantly increased serum stability, cellular transfection, synergistic cytotoxicity and apoptosis in vitro compared to normal ODNs (171).…”

Section: Other Strategies In Targeting Stat3/5mentioning

confidence: 99%

“…A hybrid of lipid and polymer vesicles with calcium phosphate as the solid kernel (CaP@HA) was used to introduce STAT3-specific decoy oligonucleotides (STAT3-decoy-ODNs) into TRAZ-resistant HER2-positive breast cancer cells (171). ODNs packaged with CaP@HA showed significantly increased serum stability, cellular transfection, synergistic cytotoxicity and apoptosis in vitro compared to normal ODNs (171).…”

Section: Other Strategies In Targeting Stat3/5mentioning

confidence: 99%

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Signal Transducer and Activator of Transcription (STATs) Proteins in Cancer and Inflammation: Functions and Therapeutic Implication

et al. 2019

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Signal Transducer and Activator of Transcription (STAT) pathway is connected upstream with Janus kinases (JAK) family protein and capable of integrating inputs from different signaling pathways. Each family member plays unique functions in signal transduction and crucial in mediating cellular responses to different kind of cytokines. STAT family members notably STAT3 and STAT5 have been involved in cancer progression whereas STAT1 plays opposite role by suppressing tumor growth. Persistent STAT3/5 activation is known to promote chronic inflammation, which increases susceptibility of healthy cells to carcinogenesis. Here, we review the role of STATs in cancers and inflammation while discussing current therapeutic implications in different cancers and test models, especially the delivery of STAT3/5 targeting siRNA using nanoparticulate delivery system.

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Section: Other Strategies In Targeting Stat3/5mentioning

confidence: 99%

Section: Other Strategies In Targeting Stat3/5mentioning

confidence: 99%

Signal Transducer and Activator of Transcription (STATs) Proteins in Cancer and Inflammation: Functions and Therapeutic Implication

et al. 2019

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“…C188-9 can inhibit the dimerization of STAT3 [104] and decrease the in vivo tumorigenic potential of NSCLC cells [105]. A STAT3 decoy consisting of double stranded oligonucleotides can bind to STAT3 and prevent STAT3 from binding to target gene promoters [106,107]. Buparlisib (an inhibitor of PI3K signaling) in combination with erlotinib exerts anti-tumor effects [108].…”

Section: Anti-cancer Drugs Targeting Egfr and Egfr Signalingmentioning

confidence: 99%

Targeting Autophagy for Overcoming Resistance to Anti-EGFR Treatments

Kwon

Kim

Jung

et al. 2019

Cancers

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Epidermal growth factor receptor (EGFR) plays critical roles in cell proliferation, tumorigenesis, and anti-cancer drug resistance. Overexpression and somatic mutations of EGFR result in enhanced cancer cell survival. Therefore, EGFR can be a target for the development of anti-cancer therapy. Patients with cancers, including non-small cell lung cancers (NSCLC), have been shown to response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) and anti-EGFR antibodies. However, resistance to these anti-EGFR treatments has developed. Autophagy has emerged as a potential mechanism involved in the acquired resistance to anti-EGFR treatments. Anti-EGFR treatments can induce autophagy and result in resistance to anti-EGFR treatments. Autophagy is a programmed catabolic process stimulated by various stimuli. It promotes cellular survival under these stress conditions. Under normal conditions, EGFR-activated phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase (AKT)/mammalian target of rapamycin (mTOR) signaling inhibits autophagy while EGFR/rat sarcoma viral oncogene homolog (RAS)/mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) signaling promotes autophagy. Thus, targeting autophagy may overcome resistance to anti-EGFR treatments. Inhibitors targeting autophagy and EGFR signaling have been under development. In this review, we discuss crosstalk between EGFR signaling and autophagy. We also assess whether autophagy inhibition, along with anti-EGFR treatments, might represent a promising approach to overcome resistance to anti-EGFR treatments in various cancers. In addition, we discuss new developments concerning anti-autophagy therapeutics for overcoming resistance to anti-EGFR treatments in various cancers.

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“…It was found that the absorption of MNPs by macrophages RAW264.7 was reduced to half of the original level 72 . In addition to PEG, modification with other chemicals (as shown in Table 1 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 ) can also extend the blood circulation time of NPs.…”

Section: Circulation Of Nanocarriers In Blood and Their Interactions With Resmentioning

confidence: 99%

“… Surface modification material Carrier Ref. PEG PEG-NPs, PEG-liposome 73 , 74 Chitosan Microswimmer 75 Hyaluronic acid CuS NPs, CaP NPs 76 , 77 PVMMA mPEG- b -PLA NPs 78 Cyclodextrin Porous silicon NPs 79 Folic acid, BSA Bi–Bi 2 S 3 NPs 80 Tween 80 SPIONs 81 PEO Micelle 82 Poloxamer PLA/PLGA NPs 83 , 84 HPMA Liposome 85 PVP Liposome 85 PMOX Liposome 85 PDMA Liposome 85 PAcM Liposome 85 iRGD Self-assembling nanovesicles 86 iNGR Liposome 87 Angiopep-2 PEG-PCL NPs 88 Linear TT1 peptide Iron oxide NPs 89 NPs, nanoparticles; PEG, polyethylene glycol; PLA, polylactide; PLGA, poly (lactic- co -glycolic acid); PVMMA, poly(vinyl methyl ether/maleic anhydride); BSA, bovine serum a...…”

Section: Circulation Of Nanocarriers In Blood and Their Interactions With Resmentioning

confidence: 99%

Influencing factors and strategies of enhancing nanoparticles into tumors in vivo

Zhang

Gao

Yang

et al. 2021

Acta Pharmaceutica Sinica B

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133

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The administration of nanoparticles (NPs) first faces the challenges of evading renal filtration and clearance of reticuloendothelial system (RES). After that, NPs infiltrate through the expanded endothelial space and penetrated the dense stroma of tumor microenvironment to tumor cells. As long as possible to prolong the time of NPs remaining in tumor tissue, NPs release active agent and induce pharmacological action. This review provides a comprehensive summary of the physical and chemical properties of NPs and the influence of various biological factors in tumor microenvironment, and discusses how to improve the final efficacy through adjusting the characteristics and structure of NPs. Perspectives and future directions are also provided.

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Inorganic kernel - Supported asymmetric hybrid vesicles for targeting delivery of STAT3-decoy oligonucleotides to overcome anti-HER2 therapeutic resistance of BT474R

Cited by 17 publications

References 58 publications

Signal Transducer and Activator of Transcription (STATs) Proteins in Cancer and Inflammation: Functions and Therapeutic Implication

Signal Transducer and Activator of Transcription (STATs) Proteins in Cancer and Inflammation: Functions and Therapeutic Implication

Targeting Autophagy for Overcoming Resistance to Anti-EGFR Treatments

Influencing factors and strategies of enhancing nanoparticles into tumors in vivo

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