TY - JOUR
T1 - Microbial dysbiosis and epigenetics modulation in cancer development – A chemopreventive approach
AU - Haque, Shafiul
AU - Raina, Ritu
AU - Afroze, Nazia
AU - Hussain, Arif
AU - Alsulimani, Ahmad
AU - Singh, Vineeta
AU - Mishra, Bhartendu Nath
AU - Kaul, Sanjana
AU - Kharwar, Ravindra Nath
N1 - Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2022/11
Y1 - 2022/11
N2 - An overwhelming number of research articles have reported a strong relationship of the microbiome with cancer. Microbes have been observed more commonly in the body fluids like urine, stool, mucus of people with cancer compared to the healthy controls. The microbiota is responsible for both progression and suppression activities of various diseases. Thus, to maintain healthy human physiology, host and microbiota relationship should be in a balanced state. Any disturbance in this equilibrium, referred as microbiome dysbiosis becomes a prime cause for the human body to become more prone to immunodeficiency and cancer. It is well established that some of these microbes are the causative agents, whereas others may encourage the formation of tumours, but very little is known about how these microbial communications causing change at gene and epigenome level and trigger as well as encourage the tumour growth. Various studies have reported that microbes in the gut influence DNA methylation, DNA repair and DNA damage. The genes and pathways that are altered by gut microbes are also associated with cancer advancement, predominantly those implicated in cell growth and cell signalling pathways. This study exhaustively reviews the current research advancements in understanding of dysbiosis linked with colon, lung, ovarian, breast cancers and insights into the potential molecular targets of the microbiome promoting carcinogenesis, the epigenetic alterations of various potential targets by altered microbiota, as well as the role of various chemopreventive agents for timely prevention and customized treatment against various types of cancers.
AB - An overwhelming number of research articles have reported a strong relationship of the microbiome with cancer. Microbes have been observed more commonly in the body fluids like urine, stool, mucus of people with cancer compared to the healthy controls. The microbiota is responsible for both progression and suppression activities of various diseases. Thus, to maintain healthy human physiology, host and microbiota relationship should be in a balanced state. Any disturbance in this equilibrium, referred as microbiome dysbiosis becomes a prime cause for the human body to become more prone to immunodeficiency and cancer. It is well established that some of these microbes are the causative agents, whereas others may encourage the formation of tumours, but very little is known about how these microbial communications causing change at gene and epigenome level and trigger as well as encourage the tumour growth. Various studies have reported that microbes in the gut influence DNA methylation, DNA repair and DNA damage. The genes and pathways that are altered by gut microbes are also associated with cancer advancement, predominantly those implicated in cell growth and cell signalling pathways. This study exhaustively reviews the current research advancements in understanding of dysbiosis linked with colon, lung, ovarian, breast cancers and insights into the potential molecular targets of the microbiome promoting carcinogenesis, the epigenetic alterations of various potential targets by altered microbiota, as well as the role of various chemopreventive agents for timely prevention and customized treatment against various types of cancers.
KW - Cancer
KW - Chemoprevention
KW - DNA damage
KW - Dysbiosis
KW - Epigenetics
KW - Microbiome
UR - https://www.scopus.com/pages/publications/85109106284
U2 - 10.1016/j.semcancer.2021.06.024
DO - 10.1016/j.semcancer.2021.06.024
M3 - Artículo de revisión
C2 - 34216789
AN - SCOPUS:85109106284
SN - 1044-579X
VL - 86
SP - 666
EP - 681
JO - Seminars in Cancer Biology
JF - Seminars in Cancer Biology
ER -