PMID- 24921216
OWN - NLM
STAT- MEDLINE
DCOM- 20150514
LR  - 20140804
IS  - 1543-8392 (Electronic)
IS  - 1543-8384 (Linking)
VI  - 11
IP  - 8
DP  - 2014 Aug 4
TI  - Nanomaterial-induced autophagy: a new reversal MDR tool in cancer therapy?
PG  - 2527-38
LID - 10.1021/mp500066v [doi]
AB  - Most of the therapeutic strategies to counteract cancer imply killing of 
      malignant cells. The most exploited cell death mechanism in cancer therapies is 
      apoptosis, but recently, a lot of papers report that other mechanisms, mainly 
      autophagy, could represent a new line of attack in the fight against cancer. One 
      of the limitations for the effectiveness of the approved clinical treatments is 
      the phenomenon of multidrug resistance (MDR) which enables the cancer cells to 
      develop resistance to therapy, especially for chemotherapy. The MDR mechanisms 
      include (a) decreased uptake of drug, (b) reduced intracellular drug 
      concentration by efflux pumps, (c) altered cell cycle checkpoints, (d) altered 
      drug targets, (e) increased metabolism of drugs, (f) induced emergency response 
      genes to impair apoptotic pathway, and (g) altered drug detoxification. Great 
      efforts have been made to reverse MDR. Currently, autophagy and nanosized drug 
      delivery systems (DDSs) belonging to nanomaterials (NMs) provide alternative 
      strategies to circumvent MDR. Nanosized DDSs are very promising tools to 
      accumulate chemotherapeutics at targeting sites and control temporal and spatial 
      drug release into tumor cells. On the other hand, autophagy could overrule drug 
      resistance upon its activation by ensuring cell death via switching its 
      prosurvival role to a prodeath one or by mediating the occurrence of cell death, 
      i.e., apoptosis or necrosis. Likewise, the autophagy inhibition could counteract 
      MDR by sensitizing the cells to anticancer molecules, i.e., Src family tyrosine 
      kinase (SFK) inhibitors or 5-fluorouracil. Noteworthy, autophagy has been 
      recently indicated to be a common cellular response to NMs, corroborating the 
      fascinating idea of the exploitation of NM-induced autophagy in nanomedicine 
      therapy. This review focuses on recently published literature about the 
      relationship between MDR reversal and NMs or autophagy pointing to hypothesize a 
      pivotal role of autophagy modulation induced by NMs in counteracting MDR.
FAU - Panzarini, Elisa
AU  - Panzarini E
AD  - Department of Biological and Environmental Science and Technology (Di.S.Te.B.A.), 
      University of Salento , 73100 Lecce, Italy.
FAU - Dini, Luciana
AU  - Dini L
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140620
PL  - United States
TA  - Mol Pharm
JT  - Molecular pharmaceutics
JID - 101197791
RN  - 0 (Antineoplastic Agents)
SB  - IM
MH  - Antineoplastic Agents/pharmacology
MH  - Apoptosis
MH  - *Autophagy
MH  - Cell Line
MH  - Cell Line, Tumor
MH  - Drug Delivery Systems
MH  - *Drug Resistance, Multiple
MH  - *Drug Resistance, Neoplasm
MH  - Humans
MH  - Nanomedicine/methods
MH  - Nanostructures/*chemistry
MH  - Nanotechnology/methods
MH  - Neoplasms/*drug therapy/pathology
EDAT- 2014/06/13 06:00
MHDA- 2015/05/15 06:00
CRDT- 2014/06/13 06:00
PHST- 2014/06/13 06:00 [entrez]
PHST- 2014/06/13 06:00 [pubmed]
PHST- 2015/05/15 06:00 [medline]
AID - 10.1021/mp500066v [doi]
PST - ppublish
SO  - Mol Pharm. 2014 Aug 4;11(8):2527-38. doi: 10.1021/mp500066v. Epub 2014 Jun 20.