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

Gul-e-Saba Chaudhry; Abdah Akim; Muhammad Naveed Zafar; MA Abdullah; Yeong Yik Sung; Tengku Sifzizul Tengku Muhammad

doi:10.4103/japtr.JAPTR_26_20

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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

Gul-e-Saba Chaudhry¹, Abdah Akim², Muhammad Naveed Zafar³, MA Abdullah⁴, Yeong Yik Sung⁴, Tengku Sifzizul Tengku Muhammad⁴
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

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/japtr.JAPTR_26_20

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.

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