Epigenetics Regulation of Lung Cancer: Implications for Clinical Doctor
PDF (Spanish)

Keywords

epigenetic repression, DNA methylation, histone code, lung neoplasms, chromatin.

How to Cite

Epigenetics Regulation of Lung Cancer: Implications for Clinical Doctor. (2017). Universitas Medica, 57(3), 332-347. https://doi.org/10.11144/Javeriana.umed57-3.recp
Almetrics
 
Dimensions
 

Google Scholar
 
Search GoogleScholar

Abstract

Lung cancer is the leading cause of malingnancy death worldwide. This phenomenon occurs
when detected in the most advanced stages of the
disease (stage III or IV). There are risk factors
described in the generation of this cancer such
us the consumption of tabacco, inhalation and
subsequent accumulation of radon and asbestos
in lung tissue, environmental pollution, the presence of genetic alterations, and the presence of
epigenetic factors regulating the expression or
repression of genes involved in tumor development. Epigenetic regulation mechanisms may
get involved in tumor progression. They are
DNA methylation, histone covalent modification
and the presence of noncoding RNAs. At different stages of tumor progression it described, the
involve of epigenetic mechanisms as regulators
of processes related to proliferation, epithelial
mesenchymal transition, metastasis, apoptosis,
and others describes different stages of the tumor
progression. This review focuses on describing
the role of epigenetics in the progression of the
lung tumor and remarks on the importance of enhancing knowledge in this discipline for diagnosis and treatment

PDF (Spanish)

Curado MP, Edwards B, Shin HR, Storm

H, Ferlay J, Heanue M, Boyle P. Cancer

incidence in five continents. Vol.IX. Lyon: IARC Scientific Publications;

Forman D, Bray F, Brewster DH, Gombe

Mbalawa C, Kohler B, Piñeros M,

Steliarova-Foucher E, Swaminathan R,

Ferlay J, editors. Cancer incidence in

five continents [internet]. Vol. X. Lyon:

Insternational Agency for Research on

Cancer (IARC). Disponible en: http://

ci5.iarc.fr

Pardo C, Cendales R. Incidencia, mortalidad

y prevalencia de cáncer en Colombia,

-2011. Bogotá: Instituto Nacional de

Cancerología; 2015.

Sholl LM. Biomarkers in lung adenocarcinoma:

a decade of progress. Arch

Pathol Lab Med. 2015;139:469-5.

Hsieh T, Fischer R. Biology of chromatin

dynamics. Annu Rev Plant Biol.

;327-51.

Allis D, Caparros M, Jenuwein T, Reinberg

D. Epigenetics. 2nd ed. New York:

Cold Spring Harbor Laboratory Press;

Langevin S, Kratze R, Kelsey K. Epigenetics

of lung cancer. Transl Res.

Jan;165(1):74-90. doi: 10.1016/j.

trsl.2014.03.001

Cheng X. Blumenthal R. Coordinated

chromatin control: structural and

functional linkage of DNA and histone

methylation. Biochemistry. 2010 Apr

;49(14):2999-3008.

Liloglou T, Bediaga N, Brown B, Field

J, Davies M. Epigenetic biomarkers

in lung cancer. Cancer Lett. 2012 Jan

;342(2):200-12.

La Salle J, Trasler J. Dynamic expression

of DNMT3a and DNMT3b isoforms during

male germ cell development in the

mouse. Dev Biol. 2006;296:71-8.

Rodríguez M, Ascencia N. Metilación

del ADN: un fenómeno epigenético de

importancia médica. Rev Invest Clín.

;56(1):56-7.

Mehta A, Dobersch S, Romero A, Barreto

G. Epigenetics in lung cancer diagnosis

and therapy. Cancer Metastasis Rev.

Jun;34(2):229-41.

Glazer A, Smith M, Ochs M. Integrative

discovery of epigenetically depressed

cancer testis antigens in NSCLC. PLoS

One. 2009;4:e8189.

Kim H, Lee C. Expression of cancer-testis

antigens MAGE-A3/6 and NY-ESO-1

in non-small-cell lung carcinomas and

their relationship with immune cell infiltration.

Lung. 2009;187:401-11.

Kayser G, Sienel G, Kubitz B. Poor outcome

in primary non-small cell lung cancers

is predicted by transketolase TKTL1

expression. Pathology. 2011;43:719-24.

Renaud S, Pugacheva M, Delgado D. Expression

of the CTCF-paralogous cancertestis

gene, brother of the regulator of

imprinted sites (BORIS), is regulated by

three alternative promoters modulated

by CpG methylation and by CTCF and

p53 transcription factors. Nucl Acid Res.

;35:7372-88.

Hong J, Kang Y, Abdullaev Z. Reciprocal

binding of CTCF and BORIS to the NYESO-

promoter coincides with depression

of this cancer-testis gene in lung cancer

cells. Cancer Res. 2005;65:7763-74.

Esteller M. Epigenetic gene silencing in

cancer: the DNA hypermethylome. Hum

Mol Genet. 2007 Apr 15;16 Spec No

:R50-59. doi:10.1093/hmg/ddm018.

Rando O, Chang H. Genome wide views

of chromatin structure. Annu Rev Biochem.

;78:245-71

Kouzarides T. Chromatin modifications

and their function. Cell. 2007;128:693-

Zhang Q, Ramlee MK, Brunmeir R, Villanueva

CJ, Halperin D, Xu F. Dynamic

and distinct histone modifications

modulate the expression of key adipogenesis

regulatory genes. Cell Cycle.

;11(23):4310.

Stojanovicć D, Nikic D, Lazarevic K.

The level of nickel in smoker’s blood

and urine. Cent Eur J Public Health.

;12(4):187-9.

Sasaki H, Moriyama S, Nakashima Y,

Kobayashi Y, Kiriyama M, Fukai I, Yamakawa

Y, Fujii Y. Histone deacetylase

mRNA expression in lung cancer. Lung

Cancer. 2004;46:171-8.

Bartling B, Hofmann HS, Boettger T,

Hansen G, Burdach S, Silber RE, Simm

A. Comparative application of antibody

and gene array for expression profiling

in human squamous cell lung carcinoma.

Lung Cancer. 2005;49(2):145-54.

doi:10.1016/j.lungcan.2005.02.006

Minamiya Y, Ono T, Saito H, Takahashi

N, Ito M, Motoyama S, Ogawa J. Strong

expression of HDAC3 correlates with

a poor prognosis in patients with adenocarcinoma

of the lung. Tumour Biol.

;31(5):533-9. doi: 10.1007/s13277-

-0066-0.

Yanaihara N, Caplen N, Bowman E,

Seike M, Kumamoto K, Yi M, et al.

Unique MicroRNA molecular profiles

in lung cancer diagnosis and prognosis.

Cancer Cell. 2006;9(3):189-98.

Yu SL, Chen HY, Chang GC, Chen CY,

Chen HW, Singh S, et al. MicroRNA

signature predicts survival and relapse in

lung. Cancer Cell. 2008;13(1):48-57. doi:

1016/j.ccr.2007.12.008

Hu Z, Chen X, Zhao Y, Tian T, Jin G,

Shu Y, et al. Serum microRNA signatures

identified in a genome-wide serum

microRNA expression profiling predict

survival of non-small-cell lung cancer

J Clin Oncol. 2010;28(10):1721-6. doi:

1200/JCO.2009.24.9342

Yuan J, Yue H, Zhang M, Luo J, Liu L,

Wu W, et al. Transcriptional profiling

analysis and functional prediction of long

noncoding RNAs in cancer. Oncotarget.

Jan 23;7(7):8131-42.

Lyko F, Brown R. DNA methyltransferase

inhibitors and the development of epigenetic

cancer therapies. J Natl Cancer

Inst. 2005;97(20):1498-506.

Komashko V, Farnham P. 5-azacytidina

treatment reorganizes genomic histone

modification patterns. Epigenetics.

;5(3):229-40.

Jones DR, Moskaluk CH A, Gillenwater

HH, Petroni GR, et al. Phase I Trial of

induction histone deacetylase and proteasome

inhibition followed by surgery

in non-small cell lung cancer. J Thorac

Oncol. 2012 Nov;7(11):1683-90.

Prince HM, Bishton MJ, Harrison SJ.

Clinical studies of histone deacetylase

inhibitors. Clin Cancer Res. 2009;

:3958-69.

Glozak MA, Sengupta N, Zhang X, Seto

E. Acetylation and deacetylation of nonhistone

proteins. Gene. 2005;363:15-23.

Kim SC, Sprung R, Chen Y, Xu Y, Ball

H, Pei J, et al. Substrate and functional

diversity of lysine acetylation revealed

by aproteomics survey. Mol Cell.

;23(4):607-18.

Lane AA, Chabner BA. Histone deacetylase

inhibitors in cancer therapy. J Clin

Oncol. 2009;27:5459-68.

Langevin S, Kratzke R, Kelsey K. Epigenetics

of lung cancer. Transl Res. 2015

Jan;165(1):74-90.

Mayo MW, Denlinger CE, Broad RM,

Yeung F, Reilly ET, Shi Y, et al. Ineffectiveness

of HDAC inhibitors to induce

apoptosis involves the transcriptional

activation of NF-κB through the Akt

pathway. J Biol Chem. 2003;278:

-9.

McLaughlin KAJ, I Stasik, KM Prise,

PG Johnston, DB Longley. The

HDAC inhibitor vorinostat (SAHA)

down-regulates C-FLIP and sensitizes

human non-small cell lung carcinoma

cell lines to ionising radiation. European

Journal of Cancer. 2012;48(Suppl

:S272-3. doi:http://dx.doi.org/10.1016/

S0959-8049(12)71732-X

Riley JS, Hutchinson R, McArt DG,

Crawford N, Holohan C, Paul I, et al.

Prognostic and therapeutic relevance

of FLIP and procaspase-8 overexpression

in non-small cell lung cancer. Cell

Death Dis. 2013;4:e951. doi: 10.1038/

cddis.2013.481.

Gray JE, Haura E, Chiappori A, Tanvetyanon

T, Williams CC, Pinder-Schenck

M, A phase I, pharmacokinetic and pharmacodynamic

study of panobinostat, an

HDAC inhibitor, combinedwith erlotinib

in patients with advanced aerodigestive

tract tumors. Clin Cancer Res. 2014 Mar

;20(6):1644-55.

Greve G, Schiffmann I, Pfeifer D, Pantic

M, Schüler J, Lübbert M. The pan-HDAC

inhibitor panobinostat acts as a sensitizer

for erlotinib activity in EGFR-mutated

and -wildtype non-small cell lung cancer

cells. BMC Cancer. 2015;15:947.

Reguart N, Rosell R, Cardenal F, Cardona

AF, Isla D, Palmero R, et al. Phase I/

II trial of vorinostat (SAHA) and erlotinib

for non-small cell lung cancer (NSCLC)

patients with epidermal growth

factor receptor (EGFR) mutations after

erlotinib progression. Lung Cancer. 2014

May;84(2):161-7.

Trédaniel R, Descourt D, Moro-Sibilot

J, Misset E, Gachard J, Garcia-Vargas

E, et al. Vorinostat in combination with

gemcitabine and cisplatinum in patients

with advanced non-small cell lung cancer

(NSCLC): A Phase I dose-escalation study.

J Clin Oncol. 2009;27:35-7.

Ramalingam SS, Maitland ML, Frankel

P, Argiris AE, Koczywas M, Gitlitz B, et

al. Carboplatin and Paclitaxel in combination

with either vorinostat or placebo

for first-line therapy of advanced nonsmall-

cell lung cancer. J Clin Oncol.

;28(1):56-62.

Juergens RA, Wrangle J, Vendetti FP,

Murphy SC, Zhao M, Coleman B, et

al. Combination epigenetic therapy

has efficacy in patients with refractory

advanced non-small cell lung cancer.

Cancer Discov. 2011;1(7):598-607. doi:

1158/2159-8290.

ClinicalTrials.gov. Ph1b/2 Dose-Escalation

Study of Entinostat with Pembrolizumab

in NSCLC with Expansion Cohorts

in NSCLC and Melanoma [internet].

NCT02437136. Disponible en: https://clinicaltrials.

gov/ct2/show/NCT02437136

This journal is registered under a Creative Commons Attribution 4.0 International Public License. Thus, this work may be reproduced, distributed, and publicly shared in digital format, as long as the names of the authors and Pontificia Universidad Javeriana are acknowledged. Others are allowed to quote, adapt, transform, auto-archive, republish, and create based on this material, for any purpose (even commercial ones), provided the authorship is duly acknowledged, a link to the original work is provided, and it is specified if changes have been made. Pontificia Universidad Javeriana does not hold the rights of published works and the authors are solely responsible for the contents of their works; they keep the moral, intellectual, privacy, and publicity rights.

Approving the intervention of the work (review, copy-editing, translation, layout) and the following outreach, are granted through an use license and not through an assignment of rights. This means the journal and Pontificia Universidad Javeriana cannot be held responsible for any ethical malpractice by the authors. As a consequence of the protection granted by the use license, the journal is not required to publish recantations or modify information already published, unless the errata stems from the editorial management process. Publishing contents in this journal does not generate royalties for contributors.