Journal
ADVANCED MATERIALS
Volume 31, Issue 35, Pages -Publisher
WILEY-V C H VERLAG GMBH
DOI: 10.1002/adma.201902952
Keywords
cancer treatment; immunotherapy; liposomes; macrophages; ovarian cancer
Categories
Funding
- National Science Foundation [CBET-1603177, ECCS-1542148] Funding Source: Medline
- NCI NIH HHS [R01 CA226909, P30 CA023100, R56 CA207839, R01 CA188883, P30CA23100, R01 CA167426] Funding Source: Medline
- NIAID NIH HHS [R01 AI132413] Funding Source: Medline
- NIDCR NIH HHS [R01 DE027325] Funding Source: Medline
- NIH HHS [R01 AI132413-01, S10 OD023527] Funding Source: Medline
- University of California, San Diego Funding Source: Medline
- National Nanotechnology Coordinated Infrastructure Funding Source: Medline
- University of CaliforniaSan Diego's Dissertation Fellowship Funding Source: Medline
- San Diego Nanotechnology Infrastructure Funding Source: Medline
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Despite the promise of ribonucleic acid interference therapeutics, the delivery of oligonucleotides selectively to diseased tissues in the body, and specifically to the cellular location in the tissues needed to provide optimal therapeutic outcome, remains a significant challenge. Here, key material properties and biological mechanisms for delivery of short interfering RNAs (siRNAs) to effectively silence target-specific cells in vivo are identified. Using porous silicon nanoparticles as the siRNA host, tumor-targeting peptides for selective tissue homing, and fusogenic lipid coatings to induce fusion with the plasma membrane, it is shown that the uptake mechanism can be engineered to be independent of common receptor-mediated endocytosis pathways. Two examples of the potential broad clinical applicability of this concept in a mouse xenograft model of ovarian cancer peritoneal carcinomatosis are provided: silencing the Rev3l subunit of polymerase Pol zeta to impair DNA repair in combination with cisplatin; and reprogramming tumor-associated macrophages into a proinflammatory state.
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