Scriptaid cause histone deacetylase inhibition and cell cycle arrest in HeLa cancer cells: A study on structural and functional aspects

  • Gene. 2017 Sep 5;627:379-386. doi: 10.1016/j.gene.2017.06.031.
M Janaki Ramaiah  1 ,  Shaik Mohammad Naushad  2 ,  A Lavanya  3 ,  Chatla Srinivas  3 ,  Tangutur Anjana Devi  3 ,  Sowganthika Sampathkumar  4 ,  Dhepikha Bharani Dharan  4 ,  Manika Pal Bhadra  5
Affiliations
  • 1. School of Chemical and Biotechnology, SASTRA University, Thanjavur 613401, India. Electronic address: [email protected].
  • 2. School of Chemical and Biotechnology, SASTRA University, Thanjavur 613401, India; Sandor Life Sciences Pvt. Ltd, Banjara Hills, Road No: 3, Hyderabad-500034, India.
  • 3. Chemical Biology Department, Indian Institute of Chemical Technology (IICT), Hyderabad 500007, India.
  • 4. School of Chemical and Biotechnology, SASTRA University, Thanjavur 613401, India.
  • 5. Chemical Biology Department, Indian Institute of Chemical Technology (IICT), Hyderabad 500007, India. Electronic address: [email protected].
PMID: 28668345 DOI: 10.1016/j.gene.2017.06.031
Abstract

Scriptaid (SCR), a well-known histone deacetylase inhibitor, cause various cellular effects such as cell growth inhibition and Apoptosis. In this study, we have evaluated the anti-cancer effects of Scriptaid in HeLa cells, IMR-32 and HepG2 cells. Scriptaid inhibited the growth of HeLa cells with IC50 of 2μM at 48h in a dose-dependent manner. Flow-cytometric analysis indicated that SCR induced Apoptosis. Scriptaid was found to inhibit HDAC-8 effectively than other HDAC Inhibitor such as TSA as observed by HDAC-8 assay, Western blotting and modelling study. This observation was further strengthened by an artificial neuronal network (ANN) model.

Keywords
ANN; HDAC; HeLa; Scriptaid.
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