Integrated Bioinformatics Approach for Disclosing Autophagy Pathway as a Therapeutic Target in Advanced KRAS Mutated/Positive Lung Adenocarcinoma

Yasmeen Dodin1, *
1 Cancer Control Office, King Hussein Cancer Center, Amman 11941, Jordan

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Creative Commons License
© 2023 Yasmeen Dodin

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Cancer Control Office, King Hussein Cancer Center, Amman 11941, Jordan; Tel: (962-6) 5300460 Ext: 2205. E-mail: YD.14502@KHCC.JO



Lung cancer is the leading cause of cancer-related deaths, accounting for 1.8 million deaths (18%). Nearly 80%-85% of lung cancer cases are non-small cell lung cancers (NSCLC). One of the most frequent genetic mutations in NSCLC is the Kirsten Rat Sarcoma Oncogene Homolog (KRAS) gene mutation. In recent years, autophagy has drawn substantial attention as a potential pathway that can be targeted in cancer driven by KRAS gene mutation to efficiently improve the therapeutic profile of different treatments.


In this study, we have investigated the potential of targeting the autophagy pathway as a treatment approach in advanced KRAS-mutated lung adenocarcinoma using gene expression data from The Cancer Genome Atlas Lung Adenocarcinoma (TCGA-LUAD) project.


Compared to KRAS wild-type lung adenocarcinoma, there were found 11 differentially expressed autophagy-related genes (DEARGs), with 5 upregulated and 6 downregulated DEARGs (threshold of adjusted p-value <0.05).


These DEARGs can be investigated as potential genes that can be targeted by different autophagy inhibitors.

Keywords: Lung adenocarcinoma (LUAD), The Cancer Genome Atlas (TCGA), Kirsten Rat Sarcoma Oncogene Homolog (KRAS), Bioinformatics analysis, Autophagy-related genes (ARGs), Autophagy inhibitors.