Home  |  About JAPTR |  Editorial board  |  Search |  Ahead of print  |  Current issue  |  Archives |  Submit article  |  Instructions  |  Subscribe  |  Advertise  |  Contacts  |Login 
Users Online: 141   Home Print this page Email this page Small font sizeDefault font sizeIncrease font size
     
ORIGINAL ARTICLE
Year : 2020  |  Volume : 11  |  Issue : 3  |  Page : 101-106

Induction of apoptosis and role of paclitaxel-loaded hyaluronic acid-crosslinked nanoparticles in the regulation of AKT and RhoA


1 Institute of Marine Biotechnology, Universiti Malaysia Terengganu, Kuala Terengganu; Department of Chemical Engineering, Universiti Teknologi Petronas, Perak, Malaysia
2 Department of Biomedical Sciences, Universiti Putra Malaysia, Seri Kembangan, Selangor, Malaysia
3 Department of Chemistry, Quaid-i-Azam University, Islamabad, Pakistan
4 Institute of Marine Biotechnology, Universiti Malaysia Terengganu, Kuala Terengganu, Malaysia

Correspondence Address:
Prof. Abdah Akim
Department of Biomedical Sciences, Universiti Putra Malaysia, Seri Kembangan, Selangor
Malaysia
Dr. Gul-e-Saba Chaudhry
Institute of Marine Biotechnology, Universiti Malaysia Terengganu, Terengganu 21030
Malaysia
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/japtr.JAPTR_26_20

Rights and Permissions

Cancer is a complex multifactorial disease and leading causes of death worldwide. Despite the development of many anticancer drugs, there is a reduced survival rate due to severe side effects. The nontargeted approach of convention drugs is one of the leading players in context to toxicity. Hyaluronan is a versatile bio-polymer and ligand of the receptor (CD44) on cancer cells. The MCF-7 and HT-29 cancer cell lines treated with hyaluronic acid-paclitaxel (HA-PTX) showed the distinguishing morphological features of apoptosis. Flow cytometric analysis showed that HA-PTX induces apoptosis as a significant mode of cell death. The activation level of tumor suppressor protein (p53) increased after PTX treatment in MCF-7, but no changes observed in HT-29 might be due to hereditary mutations. The lack of suppression in AKT and Rho A protein suggest the use of possible inhibitors in future studies which might could play a role in increasing the sensitivity of drug towards mutated cells line and reducing the possibilities for cancer cell survival, migration, and metastasis.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed339    
    Printed19    
    Emailed0    
    PDF Downloaded80    
    Comments [Add]    

Recommend this journal