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Year 2021, Volume: 42 Issue: 4, 751 - 757, 29.12.2021

Hamid Ceylan

Abstract

References

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  • [24] Luo B.L., Zhou Y., Lv H., Sun S.H., Tang W.X., MS‐275 potentiates the effect of YM‐155 in lung adenocarcinoma via survivin downregulation induced by miR‐138 and miR‐195, Thorac. Can., 10 (2019) 1355-1368.

Identification and validation of key genes associated with smoking-induced lung adenocarcinoma development through bioinformatics analysis and predictions of small-molecule drugs

Year 2021, Volume: 42 Issue: 4, 751 - 757, 29.12.2021

Hamid Ceylan

Abstract

Although smoking is known to be the leading risk factor for lung cancer, it is still unclear how normal cells turn cancerous in cigarette smokers. This study aimed to identify key molecular drivers that contributed to the progression and prognosis of lung adenocarcinoma (LUAD) in cigarette smokers, as well as screen, correlated small molecule therapeutic drugs by bioinformatics analysis. Gene expression profile was obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between current smokers without cancer and never smokers were identified and were analyzed to identify gene ontologies, pathways, protein‑protein interaction (PPI) networks, hub genes, and prognostic potentials. Finally, effective small-molecule compounds were screened by the Connectivity Map (CMap) database. A total of nine genes were screened out as the critical among the DEGs from the PPI network. Overall survival analysis revealed that high mRNA expression of ACTR2 and ANAPC10 were significantly associated with the LUAD. Furthermore, three candidate small-molecule drugs for manipulating LUAD progression were predicted. Identification of critical genes involved in disease development and candidate drugs to combat it can lead us to better diagnosis and targeted therapy strategies. The results of the present study may provide insight into the mechanisms underlying LUAD pathogenesis development risk in cigarette smokers and may provide potential targets for prevention.

Keywords

Bioinformatics analysis Differentially expressed genes Lung adenocarcinoma Overall survival Smoking.

References

  • [1] Sung H., Ferlay J., Siegel R.L., Laversanne M., Soerjomataram I., Jemal A., Bray F., Global Cancer Statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries, CA: Cancer J. Clin., 71(3) (2021) 209-249.
  • [2] Bender E., Epidemiology: the dominant malignancy, Nature, 513 (2014) S2-S3.
  • [3] Hammouz R.Y., Kostanek J.K., Dudzisz A., Witas P., Orzechowska M., Bednarek AK., Differential expression of lung adenocarcinoma transcriptome with signature of tobacco exposure, J. App. Genet., 61 (2020) 421-437.
  • [4] Herbst R.S., Morgensztern D., Boshoff C., The biology and management of non-small cell lung cancer, Nature, 553 (2018) 446-454.
  • [5] Ducray F., Honnorat J., Lachuer J., DNA microarray technology: principles and applications to the study of neurological disorders, Rev. Neurol., 163 (2007) 409-420.
  • [6] Sahin U., Derhovanessian E., Miller M., Kloke B.P., Simon P., Löwer M., Bukur V., Tadmor A.D., Luxemburger U., Schrörs B., Personalized RNA mutanome vaccines mobilize poly-specific therapeutic immunity against cancer, Nature, 547 (2017) 222-226.
  • [7] Li L., Lei Q., Zhang S., Kong L., Qin B., Screening and identification of key biomarkers in hepatocellular carcinoma: evidence from bioinformatic analysis, Oncol. Rep., 38 (2017) 2607-2618.
  • [8] Liu W., Ouyang S., Zhou Z., Wang M., Wang T., Qi Y., Zhao C., Chen K., Dai L., Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases, Mol. Genet. Gen. Med., 7 (2019) e00528.
  • [9] Wang X., Pittman G.S., Bandele O.J., Bischof J.J., Liu G., Brothers J.F., Spira A., Bell D.A., Linking polymorphic p53 response elements with gene expression in airway epithelial cells of smokers and cancer risk, Hum. Genet., 133 (2014) 1467-1476.
  • [10] Tang Z., Li C., Kang B., Gao G., Li C., Zhang Z., GEPIA: a web server for cancer and normal gene expression profiling and interactive analyses, Nucleic Acids Res., 45 (2017) W98-W102.
  • [11] Győrffy B., Surowiak P., Budczies J., Lánczky A., Online survival analysis software to assess the prognostic value of biomarkers using transcriptomic data in non-small-cell lung cancer, PLoS One., 8 (2013) e82241.
  • [12] World Health Organization, Noncommunicable Diseases Country Profiles – WHO Global Report, Geneva: WHO, (2018).
  • [13] Forum of International Respiratory Societies. The Global Impact of Respiratory Disease – Second Edition. Sheffi eld, European Respiratory Society (2017).
  • [14] Zappa C., Mousa S.A., Non-small cell lung cancer: current treatment and future advances, Transl. Lung Cancer Res., 5 (2016) 288-300.
  • [15] Denisenko T.V., Budkevich I.N., Zhivotovsky B., Cell death-based treatment of lung adenocarcinoma, Cell Death Dis., 9 (2018) 1-14.
  • [16] Yamaguchi H., Lorenz M., Kempiak S., Sarmiento C., Coniglio S., Symons M., Segall J., Eddy R., Miki H., Takenawa T., Molecular mechanisms of invadopodium formation: the role of the N-WASP–Arp2/3 complex pathway and cofilin, J. Cell. Biol., 168 (2005) 441-452.
  • [17] Kurisu S., Suetsugu S., Yamazaki D., Yamaguchi H., Takenawa T., Rac-WAVE2 signaling is involved in the invasive and metastatic phenotypes of murine melanoma cells, Oncogene., 24 (2005) 1309-1319.
  • [18] Sawa M., Suetsugu S., Sugimoto A., Miki H., Yamamoto M., Takenawa T., Essential role of the C. elegans Arp2/3 complex in cell migration during ventral enclosure, J. Cell. Sci., 116 (2003) 1505-1518.
  • [19] Hudson A.M., Cooley L., A subset of dynamic actin rearrangements in Drosophila requires the Arp2/3 complex, J. Cell. Biol., 156 (2002) 677-687.
  • [20] Semba S., Iwaya K., Matsubayashi J., Serizawa H., Kataba H., Hirano T., Kato H., Matsuoka T., Mukai K., Coexpression of actin-related protein 2 and Wiskott-Aldrich syndrome family verproline-homologous protein 2 in adenocarcinoma of the lung, Clin. Cancer Res., 12 (2006) 2449-2454.
  • [21] Marrocco K., Criqui M.C., Zervudacki J., Schott G., Eisler H., Parnet A., Dunoyer P., Genschik P., APC/C-mediated degradation of dsRNA-binding protein 4 (DRB4) involved in RNA silencing, PLoS One., 7 (2012) e35173.
  • [22] Wang Y., Han T., Gan M., Guo M., Xie C., Jin J., Zhang S., Wang P., Cao J., Wang J-B. A novel function of anaphase promoting complex subunit 10 in tumor progression in non-small cell lung cancer, Cell Cycle., 18 (2019) 1019-1032.
  • [23] Gerson S.L., Caimi P.F., William B.M., Creger R.J., Pharmacology and molecular mechanisms of antineoplastic agents for hematologic malignancies, Hematology (Seventh Edition), Elsevier, (2018) 849-912.
  • [24] Luo B.L., Zhou Y., Lv H., Sun S.H., Tang W.X., MS‐275 potentiates the effect of YM‐155 in lung adenocarcinoma via survivin downregulation induced by miR‐138 and miR‐195, Thorac. Can., 10 (2019) 1355-1368.
There are 24 citations in total.

Details

Primary Language English
Subjects Structural Biology
Journal Section Natural Sciences
Authors

Hamid Ceylan 0000-0003-3781-4406

Publication Date December 29, 2021
Submission Date February 27, 2021
Acceptance Date October 2, 2021
Published in Issue Year 2021Volume: 42 Issue: 4

Cite

APA Ceylan, H. (2021). Identification and validation of key genes associated with smoking-induced lung adenocarcinoma development through bioinformatics analysis and predictions of small-molecule drugs. Cumhuriyet Science Journal, 42(4), 751-757.