The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Liposome-Encapsulated Doxorubicin Reverses Drug Resistance by Inhibiting P-Glycoprotein in Human Cancer Cells
Abstract
The most frequent drawback of doxorubicin is the onset of drug resistance, due to the active efflux through P-glycoprotein (Pgp). Recently formulations of liposome-encapsulated doxorubicin have been approved for the treatment of tumors resistant to conventional anticancer drugs, but the molecular basis of their efficacy is not known. To clarify by which mechanisms the liposome-encapsulated doxorubicin is effective in drug-resistant cancer cells, we analyzed the effects of doxorubicin and doxorubicin-containing anionic liposomal nanoparticles ("Lipodox") on the drug-sensitive human colon cancer HT29 cells and on the drug-resistant HT29-dx cells. Interestingly, we did not detect any difference in drug accumulation and toxicity between free doxorubicin and Lipodox in HT29 cells, but Lipodox was significantly more effective than doxorubicin in HT29-dx cells, which are rich in Pgp. This effect was lost in HT29-dx cells silenced for Pgp and acquired by HT29 cells overexpressing Pgp. Lipodox was less extruded by Pgp than doxorubicin and inhibited the pump activity. This inhibition was due to a double effect: the liposome shell per se altered the composition of rafts in resistant cells and decreased the lipid raft-associated amount of Pgp, and the doxorubicin-loaded liposomes directly impaired transport and ATPase activity of Pgp. The efficacy of Lipodox was not increased by verapamil and cyclosporin A and was underwent interference by colchicine. Binding assays revealed that Lipodox…
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Liposome-encapsulated drugs have shown lower side effects.
“As alternative strategy, liposome-encapsulated drugs that have shown selective intratumour drug delivery, lower side effects and particular efficacy against aggressive and chemoresistant tumours (Jabr-Milane et al., 2008;Riganti et al., 2011), have been proposed as vehicles able to cross the BBB (through a diffusion process or a receptor-mediated endocytosis) and deliver their cargo into the CNS (”
From The association of statins plus LDL receptor‐targeted liposome‐encapsulated doxorubicin increases in vitro drug delivery across blood–brain barrier cells (2012) · cites this paper as Riganti et al., 2011
Empty liposomes may affect different intracellular pathways modulating the activity of Pgp/ABCB1 in epithelial cells.
“Empty liposomes may affect different intracellular pathways modulating the activity of Pgp/ABCB1 in epithelial cells (Riganti et al., 2011).”
From The association of statins plus LDL receptor‐targeted liposome‐encapsulated doxorubicin increases in vitro drug delivery across blood–brain barrier cells (2012) · cites this paper as Riganti et al., 2011
Liposomal particles alter lipid composition of plasma membrane microdomains, interfere with ATP hydrolysis and substrate binding, and elicit lower extrusion of doxorubicin in Pgp-overexpressing cells.
“Besides being taken up more by LDL receptor-driven endocytosis (Kopecka et al., 2011), liposomal particles alter the lipid composition of the plasma membrane microdomains (i.e.lipid rafts) where Pgp/ABCB1 is active, interfere with ATP hydrolysis and substrate binding, and elicit a lower extrusion of doxorubicin in Pgp-overexpressing cells (Riganti et al., 2011).”
From The association of statins plus LDL receptor‐targeted liposome‐encapsulated doxorubicin increases in vitro drug delivery across blood–brain barrier cells (2012) · cites this paper as Riganti et al., 2011
Liposome-encapsulated drugs have shown particular efficacy against aggressive and chemoresistant tumours.
“As alternative strategy, liposome-encapsulated drugs that have shown selective intratumour drug delivery, lower side effects and particular efficacy against aggressive and chemoresistant tumours (Jabr-Milane et al., 2008;Riganti et al., 2011), have been proposed as vehicles able to cross the BBB (through a diffusion process or a receptor-mediated endocytosis) and deliver their cargo into the CNS (”
From The association of statins plus LDL receptor‐targeted liposome‐encapsulated doxorubicin increases in vitro drug delivery across blood–brain barrier cells (2012) · cites this paper as Riganti et al., 2011
Liposome-encapsulated drugs have shown selective intratumour drug delivery.
“As alternative strategy, liposome-encapsulated drugs that have shown selective intratumour drug delivery, lower side effects and particular efficacy against aggressive and chemoresistant tumours (Jabr-Milane et al., 2008;Riganti et al., 2011), have been proposed as vehicles able to cross the BBB (through a diffusion process or a receptor-mediated endocytosis) and deliver their cargo into the CNS (”
From The association of statins plus LDL receptor‐targeted liposome‐encapsulated doxorubicin increases in vitro drug delivery across blood–brain barrier cells (2012) · cites this paper as Riganti et al., 2011
Empty liposomal shells do not exert any permeabilizing activity on delivery of doxorubicin across BBB.
“Empty liposomal shells, which inhibited the activity of Pgp/ABCB1 in chemoresistant tumours (Riganti et al., 2011), did not exert any permeabilizing activity on the delivery of doxorubicin across the BBB”
From The association of statins plus LDL receptor‐targeted liposome‐encapsulated doxorubicin increases in vitro drug delivery across blood–brain barrier cells (2012) · cites this paper as Riganti et al., 2011
Citations
Cites
Fong, W.-F., Wan, C.-K., Zhu, G.-Y., Chattopadhyay, A., Dey, S., Zhao, Z., & Shen, X.-L. (2007) · Planta Medica · doi:10.1055/s-2007-967120 · Cited by 57
Flagged first, then by citations
Research works printed but not linked: 47
- Thomas H., 2003, Cancer Control, 10, 159, 10.1177/107327480301000207 · DOI · Paper page
- Sarkadi B., 2006, Physiol. Rev., 86, 1179, 10.1152/physrev.00037.2005 · DOI
- Borowski E., 2005, Acta Biochim. Pol., 52, 609, 10.18388/abp.2005_3421 · DOI
- Muñoz-Martínez F., 2006, Biochim. Biophys. Acta, 1758, 98, 10.1016/j.bbamem.2005.12.006 · DOI
- MacDiarmid J. A., 2009, Nat. Biotechnol., 27, 643, 10.1038/nbt.1547 · DOI
- Martin C., 2000, Mol. Pharmacol., 58, 624, 10.1124/mol.58.3.624 · DOI
- Markman M., 2006, Expert Opin. Pharmacother., 7, 1469, 10.1517/14656566.7.11.1469 · DOI
- Glas M., 2007, Oncology, 72, 302, 10.1159/000113052 · DOI · Paper page
- Jabr-Milane L. S., 2008, Cancer Treat. Rev., 34, 592, 10.1016/j.ctrv.2008.04.003 · DOI
- Rajendran L., 2010, Nat. Rev. Drug Discovery, 9, 29, 10.1038/nrd2897 · DOI
- Kobayashi T., 2007, Int. J. Pharm., 329, 94, 10.1016/j.ijpharm.2006.08.039 · DOI
- Zalipsky S., 2007, J. Drug Targeting, 15, 518, 10.1080/10611860701499946 · DOI
- Ogawara K., 2009, J. Controlled Release, 133, 4, 10.1016/j.jconrel.2008.09.008 · DOI · Paper page
- Leonard R. C. F., 2009, Breast, 18, 218, 10.1016/j.breast.2009.05.004 · DOI
- Visani G., 2009, Expert Rev. Anticancer Ther., 9, 357, 10.1586/14737140.9.3.357 · DOI
- Thierry A. R., 1993, FASEB J., 7, 572, 10.1096/fasebj.7.6.8097173 · DOI
- Rahman A., 1992, J. Natl. Cancer Inst., 84, 1909, 10.1093/jnci/84.24.1909 · DOI
- Thierry A. R., 1992, Biochem. Biophys. Res. Commun., 187, 1098, 10.1016/0006-291X(92)91310-M · DOI
- Riganti C., 2005, Cancer Res., 65, 516, 10.1158/0008-5472.516.65.2 · DOI · Paper page
- Riganti C., 2008, Eur. Respir. J., 32, 443, 10.1183/09031936.00090407 · DOI
- Wong H. L., 2004, J. Pharm. Sci., 93, 1993, 10.1002/jps.20100 · DOI
- Provencher S. W., 1982, Comput. Phys. Commun., 27, 213, 10.1016/0010-4655(82)90173-4 · DOI
- Doublier S., 2008, Mol. Cancer Res., 6, 1607, 10.1158/1541-7786.MCR-08-0251 · DOI
- Litman T., 1997, Biochim. Biophys. Acta, 1361, 169, 10.1016/S0925-4439(97)00027-6 · DOI
- Troost J., 2004, Mol. Pharmacol., 66, 1332, 10.1124/mol.104.002329 · DOI
- Omote H., 2004, Biochemistry, 43, 3917, 10.1021/bi035365l · DOI
- Mizutani T., 2005, Drug Metab. Rev., 37, 489, 10.1080/03602530500205358 · DOI
- Choi K., 1988, Cell, 53, 519, 10.1016/0092-8674(88)90568-5 · DOI
- Rao U. S., 1995, J. Biol. Chem., 270, 6686, 10.1016/S0021-9258(18)82708-9 · DOI
- Schmid B., 2007, Bioconjugate Chem., 18, 702, 10.1021/bc0602735 · DOI
- Anhorn M. G., 2008, Bioconjugate Chem., 19, 2321, 10.1021/bc8002452 · DOI
- Dalmarks M., 1981, J. Gen. Physiol., 78, 349, 10.1085/jgp.78.4.349 · DOI
- Niu G., 2010, J. Drug Targeting, 18, 468, 10.3109/10611860903508804 · DOI
- Mamot C., 2003, Drug Resist. Updates, 6, 271, 10.1016/S1368-7646(03)00082-7 · DOI
- Kang D. I., 2009, Drug Delivery, 16, 261, 10.1080/10717540902937562 · DOI
- Rosenberg M. F., 2003, J. Biol. Chem., 278, 8294, 10.1074/jbc.M211758200 · DOI
- Litman T., 1997, Biochim. Biophys. Acta, 1361, 159, 10.1016/S0925-4439(97)00026-4 · DOI
- Orlowski S., 2006, Cell. Mol. Life Sci., 63, 1038, 10.1007/s00018-005-5554-9 · DOI
- Meyer dos Santos S., 2007, Biochem. Biophys. Res. Commun., 354, 216, 10.1016/j.bbrc.2006.12.202 · DOI
- Klappe K., 2009, Chem. Phys. Lipids, 161, 57, 10.1016/j.chemphyslip.2009.07.004 · DOI
- Barta C. A., 2008, Mol. Pharmaceutics, 5, 863, 10.1021/mp800050q · DOI
- Liu L., 2001, Mol. Pharmacol., 59, 62, 10.1124/mol.59.1.62 · DOI
- Nagy H., 2004, Biochem. Biophys. Res. Commun., 315, 942, 10.1016/j.bbrc.2004.01.156 · DOI
- Friche E., 1993, Br. J. Cancer, 67, 226, 10.1038/bjc.1993.44 · DOI
- Safa A. R., 1990, Proc. Natl. Acad. Sci. U.S.A., 87, 7225, 10.1073/pnas.87.18.7225 · DOI
- Ruth A., 2001, Biochemistry, 40, 4332, 10.1021/bi001373f · DOI
- Buda G., 2010, Ann. Hematol., 89, 1133, 10.1007/s00277-010-0992-3 · DOI
Cited by
Sorted by citations
Delivery of chemotherapeutic drugs in tumour cell-derived microparticles
Tang, K., Zhang, Y., Zhang, H., Xu, P., Liu, J., Ma, J., Lv, M., Li, D., Katirai, F., Shen, G.-X., et al. (2012) · Nature Communications · doi:10.1038/ncomms2282 · Cited by 453
Pinzón‐Daza, M., Garzón, R., Couraud, P., Romero, I., Weksler, B., Ghigo, D., Bosia, A., & Riganti, C. (2012) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2012.02103.x · Cited by 84
Self-citation
Metadata
- Authors
- Riganti, C., Voena, C., Kopecka, J., Corsetto, P. A., Montorfano, G., Enrico, E., Costamagna, C., Rizzo, A. M., Ghigo, D., & Bosia, A.
- Affiliations
- Department of Genetics, Biology and Biochemistry, University of Torino, Torino, Italy
- Research Center on Experimental Medicine (Ce.R.M.S.), University of Torino and San Giovanni Battista Hospital, Torino, Italy
- Department of Molecular Science Applied to Biosystems (DISMAB), University of Milano, Milano, Italy
- National Institute of Metrologic Research, Electromagnetism Division, Quantum Research Laboratories and Nanofacility Piemonte, Torino, Italy
- Venue
- Molecular Pharmaceutics
- Publisher
- American Chemical Society (ACS)
- Published
- 2011-05-05
- Volume
- 8
- Issue
- 3
- Pages
- 683-700
- ISSN
- 1543-8384
- 1543-8392
- Cited by
- 86
- References
- 1
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
