scholarly journals Peptide Hormone Regulation of DNA Damage Responses

2020 ◽  
Vol 41 (4) ◽  
pp. 519-537
Author(s):  
Vera Chesnokova ◽  
Shlomo Melmed
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Cell Transformation ◽  
Peptide Hormone ◽  
Neoplastic Cell ◽  
Premature Aging ◽  
Endocrine Function ◽  
Hormone Regulation ◽  
Neoplastic Cell Transformation ◽  
Polypeptide Hormones

Abstract DNA damage response (DDR) and DNA repair pathways determine neoplastic cell transformation and therapeutic responses, as well as the aging process. Altered DDR functioning results in accumulation of unrepaired DNA damage, increased frequency of tumorigenic mutations, and premature aging. Recent evidence suggests that polypeptide hormones play a role in modulating DDR and DNA damage repair, while DNA damage accumulation may also affect hormonal status. We review the available reports elucidating involvement of insulin-like growth factor 1 (IGF1), growth hormone (GH), α-melanocyte stimulating hormone (αMSH), and gonadotropin-releasing hormone (GnRH)/gonadotropins in DDR and DNA repair as well as the current understanding of pathways enabling these actions. We discuss effects of DNA damage pathway mutations, including Fanconi anemia, on endocrine function and consider mechanisms underlying these phenotypes. (Endocrine Reviews 41: 1 – 19, 2020)

scholarly journals Impaired Expression of Cytoplasmic Actins Leads to Chromosomal Instability of MDA-MB-231 Basal-Like Mammary Gland Cancer Cell Line

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2151
Author(s):  
Vera Dugina ◽  
Galina Shagieva ◽  
Mariya Novikova ◽  
Svetlana Lavrushkina ◽  
Olga Sokova ◽  
...  
Keyword(s):  
Cell Line ◽  
Chromosomal Instability ◽  
Cell Transformation ◽  
Cancer Cell Line ◽  
Neoplastic Cell ◽  
Chromosome Morphology ◽  
Human Carcinoma ◽  
Actin Isoforms ◽  
Cytoplasmic Actin ◽  
Neoplastic Cell Transformation

We have shown previously that two cytoplasmic actin isoforms play different roles in neoplastic cell transformation. Namely, β-cytoplasmic actin acts as a tumor suppressor, whereas γ-cytoplasmic actin enhances malignant features of tumor cells. The distinct participation of each cytoplasmic actin in the cell cycle driving was also observed. The goal of this study was to describe the diverse roles of cytoplasmic actins in the progression of chromosomal instability of MDA-MB-231 basal-like human carcinoma cell line. We performed traditional methods of chromosome visualization, as well as 3D-IF microscopy and western blotting for CENP-A detection/quantification, to investigate chromosome morphology. Downregulation of cytoplasmic actin isoforms alters the phenotype and karyotype of MDA-MB-231 breast cancer cells. Moreover, β-actin depletion leads to the progression of chromosomal instability with endoreduplication and aneuploidy increase. On the contrary, γ-actin downregulation results not only in reduced percentage of mitotic carcinoma cells, but leads to chromosome stability, reduced polyploidy, and aneuploidy.

scholarly journals Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1

2007 ◽  
Vol 28 (9) ◽  
pp. 1918-1927 ◽  
Author(s):  
K. W. Lee ◽  
N. J. Kang ◽  
E. A. Rogozin ◽  
H.-G. Kim ◽  
Y. Y. Cho ◽  
...  
Keyword(s):  
Cell Transformation ◽  
Neoplastic Cell ◽  
Neoplastic Cell Transformation ◽  
Natural Inhibitor

scholarly journals The ATPase Domain but Not the Acidic Region of Cockayne Syndrome Group B Gene Product Is Essential for DNA Repair

1999 ◽  
Vol 10 (11) ◽  
pp. 3583-3594 ◽  
Author(s):  
Robert M. Brosh ◽  
Adayabalam S. Balajee ◽  
Rebecca R. Selzer ◽  
Morten Sunesen ◽  
Luca Proietti De Santis ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Excision Repair ◽  
Uv Light ◽  
Genetic Disorder ◽  
Cockayne Syndrome ◽  
Premature Aging ◽  
Atpase Domain ◽  
Acidic Region

Cockayne syndrome (CS) is a human genetic disorder characterized by UV sensitivity, developmental abnormalities, and premature aging. Two of the genes involved, CSA andCSB, are required for transcription-coupled repair (TCR), a subpathway of nucleotide excision repair that removes certain lesions rapidly and efficiently from the transcribed strand of active genes. CS proteins have also been implicated in the recovery of transcription after certain types of DNA damage such as those lesions induced by UV light. In this study, site-directed mutations have been introduced to the human CSB gene to investigate the functional significance of the conserved ATPase domain and of a highly acidic region of the protein. The CSB mutant alleles were tested for genetic complementation of UV-sensitive phenotypes in the human CS-B homologue of hamster UV61. In addition, theCSB mutant alleles were tested for their ability to complement the sensitivity of UV61 cells to the carcinogen 4-nitroquinoline-1-oxide (4-NQO), which introduces bulky DNA adducts repaired by global genome repair. Point mutation of a highly conserved glutamic acid residue in ATPase motif II abolished the ability of CSB protein to complement the UV-sensitive phenotypes of survival, RNA synthesis recovery, and gene-specific repair. These data indicate that the integrity of the ATPase domain is critical for CSB function in vivo. Likewise, the CSB ATPase point mutant failed to confer cellular resistance to 4-NQO, suggesting that ATP hydrolysis is required for CSB function in a TCR-independent pathway. On the contrary, a large deletion of the acidic region of CSB protein did not impair the genetic function in the processing of either UV- or 4-NQO-induced DNA damage. Thus the acidic region of CSB is likely to be dispensable for DNA repair, whereas the ATPase domain is essential for CSB function in both TCR-dependent and -independent pathways.

Neoplastic Cell Transformation by Heavy Ions

1989 ◽  
Vol 120 (3) ◽  
pp. 468 ◽  
Author(s):  
Masao Suzuki ◽  
Masami Watanabe ◽  
Keiji Suzuki ◽  
Kazushiro Nakano ◽  
Ichiro Kaneko
Keyword(s):  
Heavy Ions ◽  
Cell Transformation ◽  
Neoplastic Cell ◽  
Neoplastic Cell Transformation
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