UGC Approved Journal no 63975(19)
New UGC Peer-Reviewed Rules

ISSN: 2349-5162 | ESTD Year : 2014
Volume 12 | Issue 10 | October 2025

JETIREXPLORE- Search Thousands of research papers



WhatsApp Contact
Click Here

Published in:

Volume 11 Issue 2
February-2024
eISSN: 2349-5162

UGC and ISSN approved 7.95 impact factor UGC Approved Journal no 63975

7.95 impact factor calculated by Google scholar

Unique Identifier

Published Paper ID:
JETIR2402045


Registration ID:
532339

Page Number

a361-a369

Share This Article


Jetir RMS

Title

Drug resistance in Cancer – An attempt to overcome by Homology Modeling, Validation and Docking of Erythropoietin protein.

Abstract

The regulation of cell growth and tissue development significantly influence apoptosis, also known as programmed cell death. Carcinogenesis is accelerated and chemotherapeutic drugs become resistant due to defects in apoptotic processes. So, increased erythropoietin (EPO) enzyme level is the cause of drug resistance in cancer. This calls for specialized, tailored techniques. The focused approach is based on the understanding of the disease-causing protein. Erythropoietin (EPO) overexpression causes angiogenesis in VEGF therapy resistance. The protein sequence (Uniprot ID P01588) is used in the current work for template identification, alignment, the building of 3D model using the SWISS model, and validation. A protein's 3D structure has 93.9% of amino acids in the favorable region, 6.1% in the generously allowed zone, and 0% in the disallowed region. Cast P located the active site residues LYS167, ARG158, THR71, LYS179, ASP192, GLY185, and ARG193.These amino acids have a part in both the signaling process and the way the EPO protein attaches to its natural substrate (EPOR). If this amino acids are blocked, the drug resistance can be inhibited. Researchers investigated the phytochemicals Dentatin (DEN), Nordentatin (NORD), and Quercetin (QUE) binding affinities for the EPO protein since these substances have shown anti-proliferative effects in a variety of cancer cell lines. These calculations showed that Nordentatin had a higher affinity for binding EPO than Quercetin and Dentatin (∆G values of 7.4 and 6.8 kcal/mol, respectively), but also suggest that all three compounds can block erythropoietin and overcome resistance.

Key Words

Cancer, Drug resistance, Phytochemical and Insilico.

Cite This Article

"Drug resistance in Cancer – An attempt to overcome by Homology Modeling, Validation and Docking of Erythropoietin protein. ", International Journal of Emerging Technologies and Innovative Research (www.jetir.org), ISSN:2349-5162, Vol.11, Issue 2, page no.a361-a369, February-2024, Available :http://www.jetir.org/papers/JETIR2402045.pdf

ISSN


2349-5162 | Impact Factor 7.95 Calculate by Google Scholar

An International Scholarly Open Access Journal, Peer-Reviewed, Refereed Journal Impact Factor 7.95 Calculate by Google Scholar and Semantic Scholar | AI-Powered Research Tool, Multidisciplinary, Monthly, Multilanguage Journal Indexing in All Major Database & Metadata, Citation Generator

Cite This Article

"Drug resistance in Cancer – An attempt to overcome by Homology Modeling, Validation and Docking of Erythropoietin protein. ", International Journal of Emerging Technologies and Innovative Research (www.jetir.org | UGC and issn Approved), ISSN:2349-5162, Vol.11, Issue 2, page no. ppa361-a369, February-2024, Available at : http://www.jetir.org/papers/JETIR2402045.pdf

Publication Details

Published Paper ID: JETIR2402045
Registration ID: 532339
Published In: Volume 11 | Issue 2 | Year February-2024
DOI (Digital Object Identifier):
Page No: a361-a369
Country: Hyderabad, Telangana, India .
Area: Science
ISSN Number: 2349-5162
Publisher: IJ Publication


Preview This Article


Downlaod

Click here for Article Preview

Download PDF

Downloads

000159

Print This Page

Current Call For Paper

Jetir RMS