Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer

Kenneth Alibek, Stephanie Irving, Zarina Sautbayeva, Ainur Kakpenova, Aliya Bekmurzayeva, Yeldar Baiken, Nurgul Imangali, Madina Shaimerdenova, Damel Mektepbayeva, Arnat Balabiyev, Aizada Chinybayeva

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The Bcl proteins play a critical role in apoptosis, as mutations in family members interfere with normal programmed cell death. Such events can cause cell transformation, potentially leading to cancer. Recent discoveries indicate that some viral proteins interfere with Bcl proteins either directly or indirectly; however, these data have not been systematically described. Some viruses encode proteins that reprogramme host cellular signalling pathways controlling cell differentiation, proliferation, genomic integrity, cell death, and immune system recognition. This review analyses and summarises the existing data and discusses how viral proteins interfere with normal pro- and anti-apoptotic functions of Bcl-2 and Bcl-xL. Particularly, this article focuses on how viral proteins, such as Herpesviruses, HTLV-1, HPV and HCV, block apoptosis and how accumulation of such interference predisposes cancer development. Finally, we discuss possible ways to prevent and treat cancers using a combination of traditional therapies and antiviral preparations that are effective against these viruses.

Original languageEnglish
Article number44
JournalInfectious Agents and Cancer
Volume9
Issue number1
DOIs
Publication statusPublished - Dec 1 2014

Fingerprint

Viral Proteins
Cell Death
Apoptosis
Viruses
Neoplasms
Proteins
Human T-lymphotropic virus 1
Herpesviridae
Antiviral Agents
Cell Differentiation
Immune System
Cell Proliferation
Mutation
Therapeutics

Keywords

  • Apoptosis
  • Bcl-2
  • Bcl-xL
  • Cancer
  • Hepatitis C virus
  • Herpesviruses
  • Human papillomavirus
  • Human T-lymphotropic virus 1
  • Signaling pathways
  • Tumor suppressor genes

ASJC Scopus subject areas

  • Infectious Diseases
  • Oncology
  • Epidemiology
  • Cancer Research

Cite this

Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer. / Alibek, Kenneth; Irving, Stephanie; Sautbayeva, Zarina; Kakpenova, Ainur; Bekmurzayeva, Aliya; Baiken, Yeldar; Imangali, Nurgul; Shaimerdenova, Madina; Mektepbayeva, Damel; Balabiyev, Arnat; Chinybayeva, Aizada.

In: Infectious Agents and Cancer, Vol. 9, No. 1, 44, 01.12.2014.

Research output: Contribution to journalArticle

Alibek, K, Irving, S, Sautbayeva, Z, Kakpenova, A, Bekmurzayeva, A, Baiken, Y, Imangali, N, Shaimerdenova, M, Mektepbayeva, D, Balabiyev, A & Chinybayeva, A 2014, 'Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer', Infectious Agents and Cancer, vol. 9, no. 1, 44. https://doi.org/10.1186/1750-9378-9-44
Alibek, Kenneth ; Irving, Stephanie ; Sautbayeva, Zarina ; Kakpenova, Ainur ; Bekmurzayeva, Aliya ; Baiken, Yeldar ; Imangali, Nurgul ; Shaimerdenova, Madina ; Mektepbayeva, Damel ; Balabiyev, Arnat ; Chinybayeva, Aizada. / Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer. In: Infectious Agents and Cancer. 2014 ; Vol. 9, No. 1.
@article{1899db9301cc4acfa8b2dbc604b23844,
title = "Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer",
abstract = "The Bcl proteins play a critical role in apoptosis, as mutations in family members interfere with normal programmed cell death. Such events can cause cell transformation, potentially leading to cancer. Recent discoveries indicate that some viral proteins interfere with Bcl proteins either directly or indirectly; however, these data have not been systematically described. Some viruses encode proteins that reprogramme host cellular signalling pathways controlling cell differentiation, proliferation, genomic integrity, cell death, and immune system recognition. This review analyses and summarises the existing data and discusses how viral proteins interfere with normal pro- and anti-apoptotic functions of Bcl-2 and Bcl-xL. Particularly, this article focuses on how viral proteins, such as Herpesviruses, HTLV-1, HPV and HCV, block apoptosis and how accumulation of such interference predisposes cancer development. Finally, we discuss possible ways to prevent and treat cancers using a combination of traditional therapies and antiviral preparations that are effective against these viruses.",
keywords = "Apoptosis, Bcl-2, Bcl-xL, Cancer, Hepatitis C virus, Herpesviruses, Human papillomavirus, Human T-lymphotropic virus 1, Signaling pathways, Tumor suppressor genes",
author = "Kenneth Alibek and Stephanie Irving and Zarina Sautbayeva and Ainur Kakpenova and Aliya Bekmurzayeva and Yeldar Baiken and Nurgul Imangali and Madina Shaimerdenova and Damel Mektepbayeva and Arnat Balabiyev and Aizada Chinybayeva",
year = "2014",
month = "12",
day = "1",
doi = "10.1186/1750-9378-9-44",
language = "English",
volume = "9",
journal = "Infectious Agents and Cancer",
issn = "1750-9378",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer

AU - Alibek, Kenneth

AU - Irving, Stephanie

AU - Sautbayeva, Zarina

AU - Kakpenova, Ainur

AU - Bekmurzayeva, Aliya

AU - Baiken, Yeldar

AU - Imangali, Nurgul

AU - Shaimerdenova, Madina

AU - Mektepbayeva, Damel

AU - Balabiyev, Arnat

AU - Chinybayeva, Aizada

PY - 2014/12/1

Y1 - 2014/12/1

N2 - The Bcl proteins play a critical role in apoptosis, as mutations in family members interfere with normal programmed cell death. Such events can cause cell transformation, potentially leading to cancer. Recent discoveries indicate that some viral proteins interfere with Bcl proteins either directly or indirectly; however, these data have not been systematically described. Some viruses encode proteins that reprogramme host cellular signalling pathways controlling cell differentiation, proliferation, genomic integrity, cell death, and immune system recognition. This review analyses and summarises the existing data and discusses how viral proteins interfere with normal pro- and anti-apoptotic functions of Bcl-2 and Bcl-xL. Particularly, this article focuses on how viral proteins, such as Herpesviruses, HTLV-1, HPV and HCV, block apoptosis and how accumulation of such interference predisposes cancer development. Finally, we discuss possible ways to prevent and treat cancers using a combination of traditional therapies and antiviral preparations that are effective against these viruses.

AB - The Bcl proteins play a critical role in apoptosis, as mutations in family members interfere with normal programmed cell death. Such events can cause cell transformation, potentially leading to cancer. Recent discoveries indicate that some viral proteins interfere with Bcl proteins either directly or indirectly; however, these data have not been systematically described. Some viruses encode proteins that reprogramme host cellular signalling pathways controlling cell differentiation, proliferation, genomic integrity, cell death, and immune system recognition. This review analyses and summarises the existing data and discusses how viral proteins interfere with normal pro- and anti-apoptotic functions of Bcl-2 and Bcl-xL. Particularly, this article focuses on how viral proteins, such as Herpesviruses, HTLV-1, HPV and HCV, block apoptosis and how accumulation of such interference predisposes cancer development. Finally, we discuss possible ways to prevent and treat cancers using a combination of traditional therapies and antiviral preparations that are effective against these viruses.

KW - Apoptosis

KW - Bcl-2

KW - Bcl-xL

KW - Cancer

KW - Hepatitis C virus

KW - Herpesviruses

KW - Human papillomavirus

KW - Human T-lymphotropic virus 1

KW - Signaling pathways

KW - Tumor suppressor genes

UR - http://www.scopus.com/inward/record.url?scp=84928747118&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84928747118&partnerID=8YFLogxK

U2 - 10.1186/1750-9378-9-44

DO - 10.1186/1750-9378-9-44

M3 - Article

AN - SCOPUS:84928747118

VL - 9

JO - Infectious Agents and Cancer

JF - Infectious Agents and Cancer

SN - 1750-9378

IS - 1

M1 - 44

ER -