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  • br The abdominal wall is a common metastatic


    The abdominal wall is a common metastatic site for abdominal malignant tumors including liver cancer, gastric cancer, and colon and rectal cancer. It is difficult to repair and reconstruct abdominal wall defects resulting from resection of abdominal wall tumors. The devel-opment of biological patches has made it possible to repair large ab-dominal defects. At present, the most widely-used patches are human acellular dermal matrix patches, which exhibit good biocompatibility and can repair abdominal wall defects. [27] However, when parts of abdominal tumors cannot be removed by R0 resection, the remaining tumor cells easily metastasize through the biological patch, which can induce a remodeling process such as the biological mesh being in-corporated into the host through the production of new site-specific tissue [28]. Therefore, our study designed a biological patch loaded with 5-FU- and rapamycin-containing nanoparticles that could repair abdominal wall defects and cause local accumulation of higher con-centrations of the drugs due to sustained drug release from the patch at the target site, resulting in inhibition of tumor growth and metastasis. In addition, large abdominal tumors often cause diabrosis, contamina-tion, or infection, and patches loaded with 22144-77-0 may be able to effectively address these issues. For other abdominal wall metastases, patches could be loaded with drugs appropriate for treatment of those tumors.
    We proposed a working model of patches loaded with 5-FU-RAPA-PLA-NP for drug delivery and release at the tumor site. Patches were first loaded with 5-FU-RAPA-PLA-NP, then placed at the tumor site where the drug could penetrate the tumor. Because of the presence of the higher concentration of drugs in the tumor microenvironment, tumor cell growth and replication were inhibited, resulting in apop-tosis.
    In conclusion, our novel biological patch loaded with drug nano-particles was able to promote repair of abdominal wall defects and inhibit tumor recurrence and metastasis, demonstrating the potential for further development of multi-effect biological patches. Further studies should focus on optimization of drug concentration and appli-cation of the patches.
    Conflict of interest statement
    We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work, there is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, or the review of, the  Biomedicine & Pharmacotherapy 117 (2019) 109048
    manuscript entitled.
    Statement of ethics
    Animal experiments conform to internationally accepted standards and have been approved by the institutional review body of Beijing Chao-Yang Hospital, Capital Medical University.
    Disclosure statement
    The authors have no conflicts of interest to declare.
    This work was supported by grants from the Beijing Natural Science Foundation (NO. 7152064), Beijing Hospitals Authority Youth Programme (code: QML20170307) and National Natural Science Foundation of China (81541155).
    We sincerely appreciate Wang Le for his excellent technical assis-tance and advice.
    M. Okada, M. Fukushima, Rapamycin enhances chemotherapy-induced cytotoxicity by inhibiting the expressions of TS and ERK in gastric cancer cells, Int. J. Cancer 126 (11) (2010) 2716–2725.
    9 Original Article
    An actionable sterol-regulated feedback loop modulates statin sensitivity in prostate cancer
    Objective: The statin family of cholesterol-lowering drugs has been shown to induce tumor-specific apoptosis by inhibiting the rate-limiting enzyme of the mevalonate (MVA) pathway, HMG-CoA reductase (HMGCR). Accumulating evidence suggests that statin use may delay pros-tate cancer (PCa) progression in a subset of patients; however, the determinants of statin drug sensitivity in PCa remain unclear. Our goal was to identify molecular features of statin-sensitive PCa and opportunities to potentiate statin-induced PCa cell death.
    Methods: Deregulation of HMGCR expression in PCa was evaluated by immunohistochemistry. The response of PCa cell lines to fluvastatin-mediated HMGCR inhibition was assessed using cell viability and apoptosis assays. Activation of the sterol-regulated feedback loop of the MVA pathway, which was hypothesized to modulate statin sensitivity in PCa, was also evaluated. Inhibition of this statin-induced feedback loop was performed using RNA interference or small molecule inhibitors. The achievable levels of fluvastatin in mouse prostate tissue were measured using liquid chromatographyemass spectrometry.