A mesoporous silica nanoparticle system with a lactose-mediated targeting effect was demonstrated to deliver a platinum(iv) prodrug for liver cancer therapy.

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In recent decades, nanoparticulate drug delivery systems have attracted extensive attention in cancer therapy for such appealing properties as small particle size, huge surface area, narrow size distribution and prolonged circulation time. Although several nanomedicines have successfully reached the clinical, evidences have proved that therapeutic efficacy isn't improved significantly, except for better toleration and less side effects. Given that the physiological abnormalities in tumors, multiple biobarriers need to be overcome before nanomedicines are delivered to the target site. Passive targeting nanoparticles ensure nanomedicines' extensive extravasation from tumor vessels via enhanced permeation and retention effect, but the diffusion distance is limited to 2-3 cell layer thicknesses. Active targeting nanoparticles tend to bind the peripheral cells of the tumor mass, hindering nanoparticles further penetration into the tumor core region. Therefore, how to improve the deep penetration of nanomedicines into tumors is a formidable task for achieving the desired anticancer therapeutic efficacy. This review demonstrates the penetration obstacles existing in tumor region for nanoparticles, summarizes the important properties of nanomedicines affecting tumor deep penetration and highlights the solutions to improve tumor deep penetration of nanoparticles.

Objective: In the present study, we aimed to investigate the potential role of fatty acid synthase (FASN) in the development and progression of colorectal cancer (CRC). Materials and methods: FASN levels were analyzed in human CRC tissues and adjacent normal tissues by Western blots and immunohistochemistry. Potential roles of FASN in regulating CRC cell proliferation and migration were examined by genetic manipulation in vitro. The molecular signaling was determined to understand the mechanisms of observed FASN effects. Results: FASN level was upregulated in CRC tissues and high expression of FASN was significantly associated with lymph node metastasis, TNM (Tumor, Node, Metastases) stage and poor prognosis in patients with CRC. Knockdown of FASN attenuated CRC cell proliferation and migration in vitro while FASN overexpression possessed the opposite effects. FASN regulated AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR) pathway in CRC cells. Conclusion: FASN enhanced CRC cell proliferation and metastasis potentially through AMPK/mTOR pathway, indicating that FASN/AMPK/mTOR signaling axis may serve as a potential target for the treatment of CRC.