Toxicological Effects of Tobacco Compounds on the Expression of Genes Involved in Actinic Cheilitis

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Authors

  • Thiago Cavalcanti Leal
  • Luiz Carlos dos Santos
  • Ana Kelly Fernandes Duarte
  • Gabriel Cerqueira Braz da Silva
  • Jéssica Alves Gomes
  • Valdemir da Conceição
  • Wellington Danilo Soares

DOI:

https://doi.org/10.17140/DOJ-5-136

Keywords:

Lip carcinoma, Oral cancer, Epithelial-mesenchymal transition

Abstract

The molecular effects of substances present in tobacco and cancer development have been well described. Morphological studies
have demonstrated tissue changes in patients with these lesions and tobacco substances. However, the effects of the tobacco
components and the development of potentially malignant lesions remain unknown.
Materials and Methods
Thus, by chemical-biological analysis, we investigated compounds present in tobacco and the expression of genes involved in the
etiopathogenesis of actinic cheilitis.
Results and Discussion
Analysis showed a ratio of 51 harmful substances present in tobacco that are involved in several biological processes that can
cause abnormal epithelial-mesenchymal transition pathway. Also, describe how cadmium can adversely affect signaling and cell
differentiation through the inhibition of specific proteins.
Conclusion
This study provides the first approach that describes how different tobacco constituents affect a vast network of biological processes
in the development of actinic cheilitis and possible progression of the lip carcinoma.

References

Daniel FI, Alves SR, Vieira DS, Biz MT, Daniel IW, Modolo F. Immunohistochemical expression of DNA methyltransferases 1, 3a, and 3b in actinic cheilitis and lip squamous cell carcinomas. J Oral Pathol Med. 2016; 45(10): 774-779. doi: 10.1111/jop.12453

Erkek E, Kazkayasi M, Bozdogan O. Acute actinic cheilitis -like chemical irritant reaction following accidental contact with ethylene glycol-favorable response to topical 1% pimecrolimus cream: A case report. Cutan Ocul Toxicol. 2008; 27: 91-95. doi: 10.1080/15569520801946938

Lopes ML, de Oliveira DH, Sarmento DJ, Queiroz LM, Miguel MC, da Silveira EJ. Correlation between cell cycle proteins and hMSH2 in actinic cheilitis and lip cancer. Arch Dermatol Res. 2016; 308: 165-171. doi: 10.1007/s00403-016-1625-z

Oliveira Alves MG, da Mota Delgado A, Balducci I, Carvalho YR, Cavalcante AS, Almeida JD. Study of MDM2 and SUMO-1 expression in actinic cheilitis and lip cancer. Arch Dermatol Res. 2014; 306: 837-841. doi: 10.1007/s00403-014-1500-8

Feltes BC, de Faria Poloni J, Notari DL, Bonatto D. Toxicologi-cal effects of the different substances in tobacco smoke on human embryonic development by a systems chemo-biology approach. PLoS One. 2013; 8: e61743. doi: 10.1371/journal.pone.0061743

de Oliveira Ribeiro A, da Silva LC, Martins-Filho PR. Prevalence of and risk factors for actinic cheilitis in Brazilian fishermen and women. Int J Dermatol. 2014; 53: 1370-1376. doi: 10.1111/ijd.12526

Lopes ML, Nonaka CF, Queiroz LM, de Souza LB, Miguel MC, da Silveira EJ. Pattern of galectins expression in actinic cheilitis with different risks of malignant transformation. J Oral Pathol Med. 2015; 45(8): 621-626. doi: 10.1111/jop.12410

Behren A, Kamenisch Y, Muehlen S, et al. Development of an oral cancer recurrence mouse model after surgical resection. Int J Oncol. 2010; 36(4): 849-855. doi: 10.3892/ijo_00000562

Lech MM, Ostrowska L. Risk of cancer development in rela-tion to oral contraception. Eur J Contracept Reprod Health Care. 2006; 11(3): 162-168. doi: 10.1080/13625180600815706

Liu W, Shi LJ, Wu L, et al. Oral cancer development in patien-ts with leukoplakia--clinicopathological factors affecting outcome. PLoS One. 2012; 7: e34773. doi: 10.1371/journal.pone.0034773

de Santana Sarmento DJ, da Costa Miguel MC, Queiroz LM, Godoy GP, da Silveira EJ. Actinic cheilitis: Clinicopathologic profi-le and association with degree of dysplasia. Int J Dermatol. 2014; 53: 466-472. doi: 10.1111/ijd.12332

Girard KR, Hoffman BL. Actinic cheilitis. Report of a case. Oral Surg Oral Med Oral Pathol. 1980; 50: 21-24.

Junqueira JL, Bonecker M, Furuse C, et al. Actinic cheilitis among agricultural workers in Campinas, Brazil. Community Dent Health. 2011; 28: 60-63.

Levi A, Wulf HC, Enk CD. Two cases of actinic cheilitis responsive to daylight-activated photodynamic therapy (DA-P-DT). Photodermatol Photoimmunol Photomed. 2013; 29: 268-271. doi: 10.1111/phpp.12057

Covani U, Marconcini S, Giacomelli L, Sivozhelevov V, Barone A, Nicolini C. Bioinformatic prediction of leader genes in human periodontitis. J Periodontol. 2008; 79(10): 1974-1983. doi: 10.1902/ jop.2008.080062

Bai C, Capell T, Berman J, et al. Bottlenecks in carotenoid biosynthesis and accumulation in rice endosperm are influenced by the precursor-product balance. Plant Biotechnol J. 2016; 14: 195- 205. doi: 10.1111/pbi.12373 Original Research | Volume 5 | Number 1|

Baker U, Okuga M, Waiswa P, et al. Bottlenecks in the imple-mentation of essential screening tests in antenatal care: Syphi-lis, HIV, and anemia testing in rural Tanzania and Uganda. Int J Gynaecol Obstet. 2015; 130(Suppl 1): S43-S50. doi: 10.1016/j. ijgo.2015.04.017

Joseph SB, Swanstrom R, Kashuba AD, Cohen MS. Bottlenecks in HIV-1 transmission: Insights from the study of founder viruses. Nat Rev Microbiol. 2015; 13: 414-425. doi: 10.1038/nrmicro3471

Wetie AGN, Shipp DA, Darie CC. Bottlenecks in proteomics. Adv Exp Med Biol. 2014; 806: 581-593. doi: 10.1007/978-3-319- 06068-2_29

Peixoto da-Silva J, Lourenco S, Nico M, Silva FH, Martins MT, Costa-Neves A. Expression of laminin-5 and integrins in actinic cheilitis and superficially invasive squamous cell carcino-mas of the lip. Pathol Res Pract. 2012; 208: 598-603. doi: 10.1016/j. prp.2012.07.004

Keereweer S, Mol IM, Kerrebijn JD, et al. Targeting integrins and enhanced permeability and retention (EPR) effect for opti-cal imaging of oral cancer. J Surg Oncol. 105: 2012; 714-718. doi: 10.1002/jso.22102

Moon Y, Kim D, Sohn H, Lim W. Effect of CD133 overex-pression on the epithelial-to-mesenchymal transition in oral cancer cell lines. Clin Exp Metastasis. 2016; 33(5): 487-496. doi: 10.1007/ s10585-016-9793-y

Patil S, Rao RS, Ganavi BS. Mesenchymal-epithelial transition in oral cancer. J Int Oral Health. 2015; 7: i-ii.

Perisanidis C, Wrba F, Brandstetter A, et al. Impact of epi-dermal growth factor receptor, mesenchymal-epithelial transition factor, and insulin-like growth factor receptor 1 expression on sur-vival of patients with oral and oropharyngeal cancer. Br J Oral Ma-xillofac Surg. 2013; 51: 234-240. doi: 10.1016/j.bjoms.2012.06.009

Vered M, Dayan D, Yahalom R, et al. Cancer-associated fibro-blasts and epithelial-mesenchymal transition in metastatic oral ton-gue squamous cell carcinoma. Int J Cancer. 2010; 127: 1356-1362. doi: 10.1002/ijc.25358

Yu CC, Chang YC. Enhancement of cancer stem-like and epi-thelial-mesenchymal transdifferentiation property in oral epithe-lial cells with long-term nicotine exposure: Reversal by targeting SNAIL. Toxicol Appl Pharmacol. 2013; 266: 459-469. doi: 10.1016/j. taap.2012.11.023

Iglesias-Linares A, Yanez-Vico RM, Gonzalez-Moles MA. Po-tential role of HDAC inhibitors in cancer therapy: Insights into oral squamous cell carcinoma. Oral Oncol. 2010; 46: 323-329. doi: 10.1016/j.oraloncology.2010.01.009

Feng W, Cai D, Zhang B, Lou G, Zou X. Combination of HDAC inhibitor TSA and silibinin induces cell cycle arrest and apoptosis by targeting survivin and cyclinB1/Cdk1 in pancreatic Original Research | Volume 5 | Number 1| de Carvalho Fraga CA, et al cancer cells. Biomed Pharmacother. 2015; 74: 257-264. doi: 10.1016/j. biopha.2015.08.017

Zhu L, Wu K, Ma S, Zhang S. HDAC inhibitors: A new radio-sensitizer for non-small-cell lung cancer. Tumori. 2015 101: 257- 262. doi: 10.5301/tj.5000347

Wang L, Li H, Ren Y, et al. Targeting HDAC with a novel inhi-bitor effectively reverses paclitaxel resistance in non-small cell lung cancer via multiple mechanisms. Cell Death Dis. 2016; 7: e2063. doi: 10.1038/cddis.2015.328

Yoon S, Eom GH. HDAC and HDAC inhibitor: From can-cer to cardiovascular diseases. Chonnam Med J. 2016; 52: 1-11. doi: 10.4068/cmj.2016.52.1.1

Wang YL, Liui HL, Fu RG, et al. HDAC inhibitor oxamflatin induces morphological changes and has strong cytostatic effects in ovarian cancer cell lines. Curr Mol Med. 2016; 16: 232-242. doi: 10. 2174/1566524016666160225151408

Willoughby CE, Reeves HL. Combination PARP and HDAC inhibition as a therapeutic strategy targeting liver cancer stem cells? Chin Clin Oncol. 2016; 5(5): 60. doi: 10.21037/cco.2016.03.21

Matakidou A, Eisen T, Houlston RS. TP53 polymorphisms and lung cancer risk: A systematic review and meta-analysis. Mutagenesis. 2003; 18: 377-385.

Dahabreh IJ, Linardou H, Bouzika P, Varvarigou V, Murray S. TP53 Arg72Pro polymorphism and colorectal cancer risk: A sys-tematic review and meta-analysis. Cancer Epidemiol Biomarkers Prev. 2010; 19: 1840-1847. doi: 1002/ijc.24603

Dahabreh IJ, Schmid CH, Lau J, Varvarigou V, Murray S, Trikalinos TA. Genotype misclassification in genetic association studies of the rs1042522 TP53 (Arg72Pro) polymorphism: A sys-tematic review of studies of breast, lung, colorectal, ovarian, and endometrial cancer. Am J Epidemiol. 2013; 177: 1317-1325. doi: 10.1093/aje/kws394

Borges LM, Ayres FM. R337H mutation of the TP53 gene as a clinical marker in cancer patients: A systematic review of literature. Genet Mol Res. 2015; 14: 17034-17043. doi: 10.1093/aje/kws394

Fenoglio-Preiser CM, Wang J, Stemmermann GN, Noffsinger A. TP53 and gastric carcinoma: A review. Hum Mutat. 2003; 21: 258-270. doi: 10.1002/humu.10180

de Assis LV, Isoldi MC. The function, mechanisms, and role of the genes PTEN and TP53 and the effects of asbestos in the development of malignant mesothelioma: A review focused on the genes’ molecular mechanisms. Tumour Biol. 2014; 35: 889-901. doi: 10.1007/s13277-013-1210-4

Fisher OM, Lord SJ, Falkenback D, Clemons NJ, Eslick GD, Lord RV. The prognostic value of TP53 mutations in oesophageal adenocarcinoma: A systematic review and meta-analysis. Gut. 2016; 66(3): 399-410. doi: 10.1136/gutjnl-2015-310888

Staack A, Schlechte H, Sachs M, Kristiansen G, Burkhardt M. Schnorr D. Clinical value of vesical leukoplakia and evaluation of the neoplastic risk by mutation analyses of the tumor suppres-sor gene TP53. Int J Urol. 2006; 13: 1092-1097. doi: 10.1111/j. 1442-2042.2006.01503.x

Barrett JR. Cadmium and breast cancer: Exposure associated with Basal-like phenotype. Environ Health Perspect. 2009; 117: A552.

Siewit CL, Gengler B, Vegas E, Puckett R, Louie MC. Cad-mium promotes breast cancer cell proliferation by potentiating the interaction between ERalpha and c-Jun. Mol Endocrinol. 2010; 24: 981-992. doi: 10.1210/me.2009-0410

Strumylaite L, Bogusevicius A, Abdrachmanovas O, et al. Cad-mium concentration in biological media of breast cancer patients. Breast Cancer Res Treat. 2011; 125: 511-517. doi: 10.1007/s10549- 010-1007-8

Julin B, Wolk A, Johansson JE, Andersson SO, Andren O, Akesson A. Dietary cadmium exposure and prostate cancer inci-dence: A population-based prospective cohort study. Br J Cancer. 2012; 107: 895-900. doi: 10.1038/bjc.2012.311

Chen C, Xun P, Nishijo M, Carter S, He K. Cadmium exposure and risk of prostate cancer: A meta-analysis of cohort and case-control studies among the general and occupational populations. Sci Rep. 2016; 6: 25814. doi: 10.1038/srep25814

Chen C, Xun P, Nishijo M, He K. Cadmium exposure and risk Submit your article to this journal | https://openventio.org/submit-manuscript/ of lung cancer: A meta-analysis of cohort and case-control studies among general and occupational populations. J Expo Sci Environ Epidemiol. 2016; doi: 10.1038/jes.2016.6

Gul’Ko IS. Zinc, copper, manganese, cadmium, cobalt and ni-ckel content in the blood, organs and tumors in cancer patients. Vopr Onkol. 1961; 7(9): 46-51.

Conway D. Oral cancer risk and smokeless tobacco products--clouded by smoke? Evid Based Dent. 2008; 9: 114-115. doi: 10.1038/ sj.ebd.6400615

Strycharz M, Polz-Dacewicz M, Gotlabek W, Swietlicki M, Ku-pisz K. Tobacco smoking as a risk factor for oral cancer. Przegl Lek. 2008; 65: 446-450.

Jayalekshmi PA, Gangadharan P, Akiba S, Nair RR, Tsuji M, Rajan B. Tobacco chewing and female oral cavity cancer risk in Karunagappally cohort, India. Br J Cancer. 2009; 100: 848-852. doi: 10.1038/sj.bjc.6604907

Varela-Lema L, Ruano-Ravina A, Juiz Crespo MA, Barros-Dios JM. Tobacco consumption and oral and pharyngeal cancer in a Spanish male population. Cancer Lett. 2010; 288: 28-35. doi: 10.1016/j.canlet.2009.06.015

Radoi L, Paget-Bailly S, Cyr D, et al. Tobacco smoking, alcohol drinking and risk of oral cavity cancer by subsite: Results of a French population-based case-control study, the ICARE study. Eur J Cancer Prev. 2013; 22: 268-276. doi: 10.1097/CEJ.0b013e3283592 Original Research | Volume 5 | Number 1|

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Published

2017-12-27

How to Cite

Thiago Cavalcanti Leal, Luiz Carlos dos Santos, Ana Kelly Fernandes Duarte, Gabriel Cerqueira Braz da Silva, Jéssica Alves Gomes, Valdemir da Conceição, & Wellington Danilo Soares. (2017). Toxicological Effects of Tobacco Compounds on the Expression of Genes Involved in Actinic Cheilitis. Dentistry, 5(1), 11–18. https://doi.org/10.17140/DOJ-5-136