Association of MYNN, TERT and TERC Gene Polymorphisms with Prostate Cancer in Turkish Population

Myoneurin regulates BMP signaling by competing with Ppm1a for Smad binding

“…Mynn is a novel member of the BTB/POZ-ZF family and is expressed in various tissues in human and mice, including cerebellum, testis, ovary, placenta, heart, brain, liver, and muscle ( Alliel et al., 2000 ). Recently, Mynn has been suggested to be involved in tumorigenesis ( Polat et al., 2019 ; Ramakrishna et al., 2010 ). However, its physiological functions during embryonic development remain poorly understood.…”

“…Moreover, NCC-specific overexpressed casmad1 not only restored the loss of pharyngeal cartilages, but also recovered most morphological abnormalities in mynn −/− mutant, suggesting both the cell-autonomous and non-cell-autonomous roles of mynn depend on its function in maintaining BMP signal activity. A number of studies have indicated that single nucleotide polymorphisms in Mynn are associated with both the development and progression in colorectal, ovarian, and bladder cancers ( Do et al., 2015 ; Houlston et al., 2010 ; Lubbe et al., 2012 ; Polat et al., 2019 ; Song et al., 2018 ). Furthermore, alterations in BMP signaling have been implicated in the pathogenesis of several tumor types including prostate, colorectal, osteosarcomas, myelomas, and breast cancers ( Blanco Calvo et al., 2009 ; Sagorny et al., 2012 ; Wang et al., 2019 ).…”

“…Because its expression is strongly elevated through increased gene copy, Mynn has been identified as one of the potential drivers in ovarian cancer ( Ramakrishna et al., 2010 ). Moreover, genotyping analysis in patients diagnosed with bladder cancer revealed a strong cumulative association between a single nucleotide polymorphism in Mynn and tumorigenesis ( Polat et al., 2019 ). Collectively, these observations suggest a potential role for Mynn throughout development and adulthood.…”

Terc Gene Cluster Variants Predict Liver Telomere Length in Mice

“…This is the first study to our knowledge demonstrating the association between this genomic region and telomere length in mice. In humans, SNPs within this cluster are the genomic predictors most consistently associated with telomere length and related disease, despite limited knowledge on the mechanism underlying this association [9][10][11][12][13][14][15][16][17]. Elaboration of this association in an animal model may thus permit critical mechanistic research, in addition to promoting understanding of between-species telomere dynamics.…”

“…Telomere length is highly heritable in human populations as a result of sequence variation in genomic networks regulating telomere length [7,8]. Variants in a gene cluster upstream-adjacent to TERC on human chromosome 3, which includes genes APRM, LRRC31, LRRC34 and MYNN, have been found to associate with telomere length [9][10][11][12][13][14], as well as related diseases, such as cancer and diabetes [9,11,[15][16][17], in several human populations by multiple independent analyses.…”