Active targeting of orthotopic glioma using biomimetic liposomes co-loaded elemene and cabazitaxel modified by transferritin.

BACKGROUND: Effective treatment of glioma requires a nanocarrier that can cross the blood-brain barrier (BBB) to target the tumor lesion. In the current study, elemene (ELE) and cabazitaxel (CTX) liposomes were prepared by conjugating liposomes with transferrin (Tf) and embedding the cell membrane proteins of RG2 glioma cells into liposomes (active-targeting biomimetic liposomes, Tf-ELE/CTX@BLIP), which exhibited effective BBB infiltration to target glioma. RESULTS: The findings showed that Tf-ELE/CTX@BLIP was highly stable. The liposomes exhibited highly significant homologous targeting and immune evasion in vitro and a 5.83-fold intake rate compared with classical liposome (ELE/CTX@LIP). Bioluminescence imaging showed increased drug accumulation in the brain and increased tumor penetration of Tf-ELE/CTX@BLIP in orthotopic glioma model nude mice. Findings from in vivo studies indicated that the antitumor effect of the Tf-ELE/CTX@BLIP led to increased survival time and decreased tumor volume in mice. The average tumor fluorescence intensity after intravenous administration of Tf-ELE/CTX@BLIP was 65.2, 12.5, 22.1, 6.6, 2.6, 1.5 times less compared with that of the control, CTX solution, ELE solution, ELE/CTX@LIP, ELE/CTX@BLIP, Tf-ELE/CTX@LIP groups, respectively. Histopathological analysis showed that Tf-ELE/CTX@BLIP were less toxic compared with administration of the CTX solution. CONCLUSION: These findings indicate that the active-targeting biomimetic liposome, Tf-ELE/CTX@BLIP, is a promising nanoplatform for delivery of drugs to gliomas.

Advances of the Research on Mechanisms of Breast Cancer Escaping from Host Immune Surveillance / 中国普外基础与临床杂志

Objective To review the mechanisms of breast cancer escaping from host immune surveillance. Methods The current literatures on the mechanisms of breast cancer cells escaping from host immune surveillance were reviewed in the following aspects: alterations of MHC-Ⅰmolecule phenotype, deficiency of costimulatory molecules, apoptosis of T-lymphocytes induced by breast cancer cells presenting Fas ligand (FasL) and TNF-related apoptosis-inducing ligand (TRAIL) and host immune tolerance induced by tumor cells. Results Loss of classical antigen-presenting human leukocyte antigen (HLA) class-Ⅰmolecules, expression of non-classical HLA class-ⅠmoleculesHLA-G, loss of costimulatory molecule B7, apoptosis of T-lymphocytes induced by tumor cells presenting FasL and TRAIL and antigen-inducing host immune tolerance were related to breast cancer escaping from immune surveillance. Conclusion Breast cancer cells escape from host immune surveillance by altering MHC-Ⅰmolecules, lacking of costimulatory molecules, inducing of apoptosis of T cells and host immune tolerance. But the factors resulting in breast cancer escaping from host immune surveillance are not yet clear and should be further studied.