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Organotin(IV)‐Loaded Mesoporous Silica as a Biocompatible Strategy in Cancer Treatment
Author(s) -
Bulatović Mirna Z.,
MaksimovićIvanić Danijela,
Bensing Christian,
GómezRuiz Santiago,
Steinborn Dirk,
Schmidt Harry,
Mojić Marija,
Korać Aleksandra,
Golić Igor,
PérezQuintanilla Damian,
Momčilović Miljana,
Mijatović Sanja,
Kaluđerović Goran N.
Publication year - 2014
Publication title -
angewandte chemie international edition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.831
H-Index - 550
eISSN - 1521-3773
pISSN - 1433-7851
DOI - 10.1002/anie.201400763
Subject(s) - apoptosis , mesoporous silica , cell growth , cancer cell , mode of action , cancer research , melanoma , chemistry , suppressor , programmed cell death , biocompatible material , mechanism of action , kinase , cancer , microbiology and biotechnology , mesoporous material , in vitro , biochemistry , biology , medicine , biomedical engineering , gene , catalysis
The strong therapeutic potential of an organotin(IV) compound loaded in nanostructured silica (SBA‐15pSn) is demonstrated: B16 melanoma tumor growth in syngeneic C57BL/6 mice is almost completely abolished. In contrast to apoptosis as the basic mechanism of the anticancer action of numerous chemotherapeutics, the important advantage of this SBA‐15pSn mesoporous material is the induction of cell differentiation, an effect unknown for metal‐based drugs and nanomaterials alone. This non‐aggressive mode of drug action is highly efficient against cancer cells but is in the concentration range used nontoxic for normal tissue. JNK (Jun‐amino‐terminal kinase)‐independent apoptosis accompanied by the development of the melanocyte‐like nonproliferative phenotype of survived cells indicates the extraordinary potential of SBA‐15pSn to suppress tumor growth without undesirable compensatory proliferation of malignant cells in response to neighboring cell death.