Substantial cell apoptosis provoked by naked PAMAM dendrimers in HER2-positive human breast cancer via JNK and ERK1/ERK2 signalling pathways.

Computational and Structural Biotechnology Journal
Hadeel KheraldineOusama Rachid

Abstract

HER2-positive breast cancer is one of its most challenging subtypes, forming around 15-25% of the total cases. It is characterized by aggressive behavior and treatment resistance. On the other hand, poly (amidoamine) (PAMAM) dendrimers are widely used in drug delivery systems and gene transfection as carriers. PAMAMs can modulate gene expression and interfere with transactivation of the human epidermal growth factor receptor family members (HER1-4). Nevertheless, the outcome of PAMAMs on HER2-positive breast cancer remains unknown. Thus, in this study, we investigated the anti-cancer effects of different generations of PAMAM dendrimers (G4 and G6) and the outcome of their surface chemistries (cationic, neutral, and anionic) on HER2-positive breast cancer cell lines, SKBR3 and ZR75. Our data showed that PAMAM dendrimers, mainly cationic types, significantly reduce cell viability in a dose-dependent manner. More significantly, PAMAMs induce substantial cell apoptosis, accompanied by the up-regulation of apoptotic markers (Bax, Caspases-3, 8 and 9) in addition to down-regulation of Bcl-2. Moreover, our data pointed out that cationic PAMAMs inhibit colony formation compared to controls and other types of PAMAMs. The molecular pathw...Continue Reading

References

Aug 13, 1999·Genes & Development·A GrossS J Korsmeyer
Aug 30, 2000·Nature·C M PerouD Botstein
Mar 4, 2003·Nature Reviews. Drug Discovery·J Milton Harris, Robert B Chess
Apr 16, 2005·The Journal of Pharmacy and Pharmacology·Jung-Hua Steven KuoHsuan Wen Chiu
Nov 22, 2005·Advanced Drug Delivery Reviews·Ruth Duncan, Lorella Izzo
Jul 13, 2006·Journal of Controlled Release : Official Journal of the Controlled Release Society·Hongtao LvJie Yan
Oct 4, 2006·Molecular Systems Biology·Alejandro Wolf-YadlinForest M White
Jan 20, 2007·Biochemical Society Transactions·D A TomaliaS Svenson
Jun 15, 2007·Journal of Materials Science. Materials in Medicine·Hu Yang, Stephanie T Lopina
Aug 9, 2008·International Journal of Nanomedicine·Wim H De Jong, Paul J A Borm
Apr 28, 2010·Toxicology and Applied Pharmacology·Pratap C NahaHugh J Byrne
Jun 29, 2010·International Journal of Pharmaceutics·Bing WangRangaramanujam M Kannan
Jan 1, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Mahdie MollazadeAbbas Alibakhshi
Jun 11, 2014·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Evandro de AzambujaThomas M Suter
Aug 30, 2014·Nanomedicine : Nanotechnology, Biology, and Medicine·Kristina Bram KnudsenMartin Roursgaard
Nov 5, 2014·Journal of Pharmaceutical Sciences·Magdalena Labieniec-Watala, Cezary Watala
Sep 25, 2015·Environmental Science and Pollution Research International·Orarat WangpraditGregor Luthe
Jun 25, 2016·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·Isabelle Durocher, Denis Girard
Jun 19, 2017·International Journal of Pharmaceutics·Rosa Maria IacobazziNunzio Denora
Jun 24, 2017·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Ioannis Gkouveris, Nikolaos G Nikitakis
Jul 17, 2018·Advances in Colloid and Interface Science·Laura J FoxWuge H Briscoe
Oct 24, 2018·International Journal of Cancer. Journal International Du Cancer·J FerlayF Bray
May 4, 2020·The Breast : Official Journal of the European Society of Mastology·Nathalie I BouwerMark-David Levin

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