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. 2021 Jan 27;6(1):33.
doi: 10.1038/s41392-020-00390-6.

Identification and construction of a novel biomimetic delivery system of paclitaxel and its targeting therapy for cancer

Xue Wang #  1 , Wanwei Zheng #  2 , Qing Shen #  3 , Yahua Wang  1 , Yujen Tseng  2 , Zhongguang Luo  2 , Xiaoyou Wang  1 , Lei Shi  3 , Chong Li  4   5   6 , Jie Liu  7
Affiliations

Identification and construction of a novel biomimetic delivery system of paclitaxel and its targeting therapy for cancer

Xue Wang et al. Signal Transduct Target Ther. .
No abstract available

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Conflict of interest statement

X.W., Q.S., W.Z., Y.W., Y.T., Z.L., X.W., and L.S. declare no competing interests. C.L. and J.L. are members of Scientific Advisory Committee of Xiamen Ginposome Pharmaceutical Co., Ltd.

Figures

Fig. 1
Fig. 1
Paclitaxel-loaded ginsenoside-anchored liposome (Ginposome-PTX) with the simple formulation and advanced functions. a Schematic view of the ginsenoside-anchored liposome (ginposome) design. b The eight representative natural ginsenosides for screening, and their effects on diphenylhexatriene (DPH) anisotropy in liposomes. These ginsenosides share similar skeletons, and all their glycosyls consisted of completely glucose units, yet with different numbers and carbon positions. Conventional cholesterol-containing liposome (CHL) was adopted as control (n = 3). c The influence of free glucose (25 mM) on the interaction between GLUT1 and Rg5 or Rh3 by surface plasma resonance (SPR) analysis. d Snapshot of the lipid bilayer of G-PTX, and the hydrogen-bond networks formed around PTX. POPC (white) and Rg5 (blue) are shown by stick, hydrogen-bonds are denoted by black dashed lines, and PTX (purple) is shown by the sphere. e, f Surface glycosyl with sufficient SASA was required for G-PTX to realize its active-targeting ability, shown by a schematic diagram and quantitative analysis by flow cytometry (n = 3; one-way ANOVA). g Size distribution and TEM image (inlet) of G-PTX. h Snapshots of G-PTX and L-PTX (conventional liposomal PTX) after 200 ns molecular dynamics simulations, respectively. Paclitaxel molecules, conventional liposome bilayer, and Rg5-anchored lipid bilayer are colored in purple, green, and light red, respectively. i In vivo distribution of different paclitaxel formulations in tumor and liver of HGC-27 xenograft mice models (n = 3; two-way ANOVA). j Direct inhibition of GLUT1 transporter via siRNA transfection reduced G-PTX uptake in HGC-27 cancer cells, by fluorescence microscopy and western blot (inlet). siRNA-GLUT1 or a scrambled siRNA (siRNA-Control) was modified by FAM (green) and G-PTX was labeled by Nile red. Scale bar, 25 μm. k Tumor growth curves in different groups on HGC-27/T and HGC-27 tumor models (n = 6; two-tailed t-test). I The in vivo antitumor effects of G-PTX and Abraxane on PDX models. The tumors at the end of the experiment were photographed (n = 6; two-tailed t-test). m The expression of autophagy-related proteins in the HCC-27/T cells treated by G-PTX, G-Blank or Abraxane (n = 3; one-way ANOVA). Data were expressed as mean ± s.d. ‖P < 0.05 versus Control, §P < 0.05 versus Control, ‡P < 0.05 versus Control. Exact P values: Abraxane versus Control, 0.046 (LC3-II), 0.0305 (Atg5), 0.0159 (Beclin1); G-Blank versus Control, 0.0316 (LC3-II), 0.0119 (p62), 0.023 (Atg5), 0.0093 (Beclin1), 0.0152 (LAMP2); G-PTX versus Control, 0.0385 (LC3-II), 0.0213 (p62), 0.0351 (Atg5), 0.0116 (Beclin1), 0.023 (LAMP2)
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