The ectopic expression of meiCT genes promotes meiomitosis and may facilitate carcinogenesis
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The ectopic expression of meiCT genes promotes meiomitosis and may facilitate carcinogenesis. / Gantchev, Jennifer; Villarreal, Amelia; Gunn, Scott; Zetka, Monique; Ødum, Niels; Litvinov, Ivan V.
In: Cell Cycle, Vol. 19, No. 8, 2020, p. 837-854.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - The ectopic expression of meiCT genes promotes meiomitosis and may facilitate carcinogenesis
AU - Gantchev, Jennifer
AU - Villarreal, Amelia
AU - Gunn, Scott
AU - Zetka, Monique
AU - Ødum, Niels
AU - Litvinov, Ivan V.
PY - 2020
Y1 - 2020
N2 - Cancer meiomitosis is defined as the concurrent activation of both mitotic and meiotic machineries in neoplastic cells that confer a selective advantage together with increased genomic instability. MeiCT (meiosis-specific cancer/testis) genes that perform specialized functions in the germline events required for the first meiotic division are ectopically expressed in several cancers. Here we describe the expression profiles of meiCT genes and proteins across a number of cancers and review the proposed mechanisms that increase aneuploidy and elicit reduction division in polyploid cells. These mechanisms are centered on the overexpression and function of meiCT proteins in cancers under various conditions that includes a response to genotoxic stress. Since meiCT genes are transcriptionally repressed in somatic cells, their target offers a promising therapeutic approach with limited toxicity to healthy tissues. Throughout the review, we provide a detailed description of the roles for each gene in the context of meiosis and we discuss proposed functions and outcomes resulting from their ectopic reactivation in cancer.
AB - Cancer meiomitosis is defined as the concurrent activation of both mitotic and meiotic machineries in neoplastic cells that confer a selective advantage together with increased genomic instability. MeiCT (meiosis-specific cancer/testis) genes that perform specialized functions in the germline events required for the first meiotic division are ectopically expressed in several cancers. Here we describe the expression profiles of meiCT genes and proteins across a number of cancers and review the proposed mechanisms that increase aneuploidy and elicit reduction division in polyploid cells. These mechanisms are centered on the overexpression and function of meiCT proteins in cancers under various conditions that includes a response to genotoxic stress. Since meiCT genes are transcriptionally repressed in somatic cells, their target offers a promising therapeutic approach with limited toxicity to healthy tissues. Throughout the review, we provide a detailed description of the roles for each gene in the context of meiosis and we discuss proposed functions and outcomes resulting from their ectopic reactivation in cancer.
KW - Meiomitosis
KW - meiosis
KW - carcinogenesis
KW - cancer testis antigens (CTA)
KW - lymphoma
KW - sezary syndrome
KW - mycosis fungoides
KW - cutaneous T-cell lymphoma (CTCL)
KW - adenocarcinoma
KW - squamous cell carcinoma (SCC)
KW - melanoma
U2 - 10.1080/15384101.2020.1743902
DO - 10.1080/15384101.2020.1743902
M3 - Review
C2 - 32223693
VL - 19
SP - 837
EP - 854
JO - Cell Cycle
JF - Cell Cycle
SN - 1538-4101
IS - 8
ER -
ID: 239807113