Preparation of bufalin-loaded pluronic polyetherimide nanoparticles, cellular uptake, distribution, and effect on colorectal cancer

Hu, Qiang; Liang, Bo; Sun, Ying; Guo, Xinhong; Bao, Yi-Jie; Xie, Donghao; Zhou, Ming; Duan, Yourong; Yin, Peihao; Peng, Zhihai

doi:10.2147/ijn.s64708

Cited by 19 publications

(13 citation statements)

References 27 publications

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“…BU, which is extracted from Chinese toad venom, is a toxic ligand with maximal antitumour effects and is a bufadienolide[ 25 – 27 ]. Modern research has found BU to have strong anti-tumour effects.…”

Section: Discussionmentioning

confidence: 99%

Bufalin reverses ABCB1-mediated drug resistance in colorectal cancer

et al. 2017

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Multidrug resistance (MDR), mainly mediated by ABCB1 transporter, is a major cause for chemotherapy failure. Bufalin (BU), an active component of the traditional Chinese medicine chan’su, has been reported to have antitumor effects on various types of cancer cells. The purpose of this present study was to investigate the reversal effect of BU on ABCB1-mediated multidrug resistance in colorectal cancer. BU at safe concentration (5, 10, 20 nM) could reverse chemosensitivity of ABCB1-overexpression HCT8/ADR, LoVo/ADR and HCT8/ABCB1 nearly back to their parental cells level. In addition, results from the drug accumulation studies revealed that BU was able to enhance intracellular accumulation of doxorubicin (DOX) and Rhodamine 123 (Rho-123) in a dose-dependent manner. Furthermore, Western blot assays showed that BU significantly inhibited the expression level of ABCB1 protein. Meanwhile, BU stimulated the ATPase activity of ABCB1, which suggested that BU might be a substrate of ABCB1. More interestingly, docking analysis predicted that BU could be docked into the large hydrophobic drug-binding cavity of human ABCB1. Importantly, BU remarkable increased the effect of DOX against the ABCB1 resistant HCT8/ADR colorectal cell xenografts in nude mice, without inducing any obvious toxicity. Overall, we concluded that BU efficiently reversed ABCB1-mediated MDR through not only inhibited the efflux function of ABCB1, but also down-regulate its protein expression, which might represent a potential and superior ABCB1 modulator in colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

Bufalin reverses ABCB1-mediated drug resistance in colorectal cancer

et al. 2017

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“…Recently, novel bufalin formulations have shown promising efficacy in xenograft tumor models [ 7 , 30 , 31 ]. Randomized, double-blind, placebo-controlled human trials are now required to assess the therapeutic value of bufalin in various cancers.…”

Section: Discussionmentioning

confidence: 99%

“…Bufalin is a digoxin-like active component of Chan Su, a traditional Chinese medicine produced from the skin and parotid venom glands of the toad [ 1 ]. Bufalin exhibits potent antitumor activities in many human cancers such as leukemia [ 2 , 3 ], hepatocellular carcinoma [ 4 , 5 ], gastric cancer [ 6 ], and colorectal cancer [ 7 ]. Moreover, bufalin sensitizes drug-resistant cancers to various chemotherapeutic agents [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Bufalin Induces Mitochondria-Dependent Apoptosis in Pancreatic and Oral Cancer Cells by Downregulating hTERT Expression via Activation of the JNK/p38 Pathway

Tian

Dai

Sun

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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Bufalin, a digoxin-like active component of the traditional Chinese medicine Chan Su, exhibits potent antitumor activities in many human cancers. Bufalin induces mitochondria-dependent apoptosis in cancer cells, but the detailed molecular mechanisms are largely unknown. hTERT, the catalytic subunit of telomerase, protects against mitochondrial damage by binding to mitochondrial DNA and reducing mitochondrial ROS production. In the present study, we investigated the effects of bufalin on the cell viability, ROS production, DNA damage, and apoptosis of CAPAN-2 human pancreatic and CAL-27 human oral cancer cells. Bufalin reduced CAPAN-2 and CAL-27 cell viability with IC50 values of 159.2 nM and 122.6 nM, respectively. The reduced cell viability was accompanied by increased ROS production, DNA damage, and apoptosis and decreased expression of hTERT. hTERT silencing in CAPAN-2 and CAL-27 cells by siRNA resulted in increased caspase-9/-3 cleavage and DNA damage and decreased cell viability. Collectively, these data suggest that bufalin downregulates hTERT to induce mitochondria-dependent apoptosis in CAPAN-2 and CAL-27 cells. Moreover, bufalin increased the phosphorylation of JNK and p38-MAPK in CAPAN-2 and CAL-27 cells, and blocking the JNK/p38-MAPK pathway using the JNK inhibitor SP600125 or the p38-MAPK inhibitor SB203580 reversed bufalin-induced hTERT downregulation. Thus, the JNK/p38 pathway is involved in bufalin-induced hTERT downregulation and subsequent induction of apoptosis by the mitochondrial pathway.

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“…Body (Fig. 1A ) length 16.0, carapace 7.9 long, 5.0 wide, abdomen 8.8 long, 5.8 wide (data from original description by Yin et al 1997 : 64). Carapace dark reddish brown.…”

Section: Taxonomymentioning

confidence: 99%

Redescription of holotypes of four Alopecosa species (Araneae, Lycosidae) from China

Tang¹,

Xu²,

Yin³

et al. 2020

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The holotypes of four species of Alopecosa Sundevall, 1833 described from China, A. disca Tang, Yin & Yang, 1997 (♀); A. orbisaca Peng, Yin, Zhang & Kim, 1997 (♀); A. wenxianensis Tang, Yin & Yang, 1997 (♂), and A. xilinensis Peng, Yin, Zhang & Kim, 1997 (♀), are reexamined. Detailed descriptions, illustrations, remarks, and a distribution map of the three valid species are given. Alopecosa xilinensissyn. nov. is found to be junior synonym of Alopecosa licenti (Schenkel, 1953).

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Preparation of bufalin-loaded pluronic polyetherimide nanoparticles, cellular uptake, distribution, and effect on colorectal cancer

Cited by 19 publications

References 27 publications

Bufalin reverses ABCB1-mediated drug resistance in colorectal cancer

Bufalin reverses ABCB1-mediated drug resistance in colorectal cancer

Bufalin Induces Mitochondria-Dependent Apoptosis in Pancreatic and Oral Cancer Cells by Downregulating hTERT Expression via Activation of the JNK/p38 Pathway

Redescription of holotypes of four Alopecosa species (Araneae, Lycosidae) from China

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