Li Chufeng, Chen Qinjun, Jiang Chen
Department of Pharmaceutics, School of Pharmacy, Fudan University, Key Laboratory of Smart Drug Delivery, Ministry of Education, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai 201203, China.
Department of Pharmaceutics, School of Pharmacy, Fudan University, Key Laboratory of Smart Drug Delivery, Ministry of Education, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai 201203, China.
J Control Release. 2024 Sep;373:879-889. doi: 10.1016/j.jconrel.2024.07.058. Epub 2024 Aug 5.
As a key pathological feature of pancreatic ductal adenocarcinoma(PDAC), the dense extracellular matrix(ECM) limits the penetration of chemotherapy drugs and is involved in the formation of immunosuppressive microenvironment. Meanwhile, clinical practice has shown that the treatment strategy for ECM should consider its restriction of tumor cell metastasis, and the need for in-depth chemotherapy without destroying ECM is proposed. STAT3 inhibitors have been reported to regulate tumor microenvironment including interrupt the form of ECM. Therefore, we designed and established a micelle system MP@HA with in vivo targeting and responsive drug release function co-loading gemcitabine monophosphate and STAT3 inhibitor silibinin. The hyaluronic acid on the surface of the micelle can bind specifically to the CD44 molecule on the surface of tumor cells and help micelles accumulate at the tumor site. The nitroimidazole used to modify the polymeric skeleton can make the micellar structure collapse in response to hypoxia reduction conditions in the tumor environment, and release silibinin to widely regulate STAT3 molecules in the PDAC microenvironment. The polymer fragment attached with gemcitabine monophosphate can penetrate deep into PDAC tumors due to its small size and positive charge exposed, achieving deep chemotherapy. This research indicates a promising micelle system meeting complicated demands proposed in PDAC treatment to improve antitumor efficacy.
作为胰腺导管腺癌(PDAC)的关键病理特征,致密的细胞外基质(ECM)限制了化疗药物的渗透,并参与免疫抑制微环境的形成。同时,临床实践表明,针对ECM的治疗策略应考虑其对肿瘤细胞转移的限制,并提出了在不破坏ECM的情况下进行深入化疗的需求。据报道,STAT3抑制剂可调节肿瘤微环境,包括阻断ECM的形成。因此,我们设计并建立了一种具有体内靶向和响应性药物释放功能的胶束系统MP@HA,其共负载单磷酸吉西他滨和STAT3抑制剂水飞蓟宾。胶束表面的透明质酸可与肿瘤细胞表面的CD44分子特异性结合,帮助胶束在肿瘤部位积聚。用于修饰聚合物骨架的硝基咪唑可使胶束结构在肿瘤环境中缺氧条件下响应塌陷,并释放水飞蓟宾以广泛调节PDAC微环境中的STAT3分子。附着有单磷酸吉西他滨的聚合物片段因其小尺寸和暴露的正电荷可深入渗透到PDAC肿瘤中,实现深度化疗。本研究表明了一种有前景的胶束系统,可满足PDAC治疗中提出的复杂需求,以提高抗肿瘤疗效。