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. 2020 Jul-Sep;11(3):101-106.
doi: 10.4103/japtr.JAPTR_26_20. Epub 2020 Jul 14.

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

Gul-E-Saba Chaudhry  1   2 , Abdah Akim  3 , Muhammad Naveed Zafar  4 , M A Abdullah  1 , Yeong Yik Sung  1 , Tengku Sifzizul Tengku Muhammad  1
Affiliations

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

Gul-E-Saba Chaudhry et al. J Adv Pharm Technol Res. 2020 Jul-Sep.

Abstract

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.

Keywords: AKT; Rho A; apoptosis; drug delivery; flow cytometry; hyaluronan; paclitaxel.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1
Figure 1
Morphology of breast cancer cell line (MCF-7) for (a) control; (b and c) paclitaxel and hyaluronic acid-paclitaxel treated at 1 ng/ml; (d and e) paclitaxel and hyaluronic acid-paclitaxel treated at 100 ng/ml; colorectal cancer cell line (HT-29) for (f) control; (g and h) paclitaxel and hyaluronic acid-paclitaxel treated at 1 ng/ml; (i and j) paclitaxel and hyaluronic acid-paclitaxel treated at 100 ng/ml after 24 h
Figure 2
Figure 2
Flow cytometric analysis of breast cancer cell line (MCF-7) for (a) control; (b and c) paclitaxel and hyaluronic acid-paclitaxel treated at 1 ng/ml; (d and e) paclitaxel and hyaluronic acid-paclitaxel treated at 100 ng/ml; colorectal cancer cell line (HT-29) for (f) control; (g and h) paclitaxeland hyaluronic acid-paclitaxel treated at 1 ng/ml; (i and j) paclitaxel and hyaluronic acid-paclitaxel treated at 100 ng/ml after 24 h
Figure 3
Figure 3
Adenosine diphosphate/adenosine triphosphate ratio in breast and colorectal cancer cell lines treatment at 1 and 100 ng/ml treatment after 24 h
Figure 4
Figure 4
p53 activation in breast and colorectal cancer cell lines after paclitaxeland hyaluronic acid-paclitaxel treatment at 1 and 100 ng/ml treatment after 24 h
Figure 5
Figure 5
AKT activation in breast and colorectal cancer cell lines treatment at 1 and 100 ng/ml treatment after 24 h
Figure 6
Figure 6
Rho A activation in breast and colorectal cancer cell lines after paclitaxel and hyaluronic acid-paclitaxel treatment at 1 and 100 ng/ml treatment after 24 h
See this image and copyright information in PMC

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