Cell proliferation and DNA repair in the liver during early stages of chemical carcinogenesis

1985 ◽  
Vol 23 ◽  
pp. 241-262 ◽  
Author(s):  
H.M. Rabes ◽  
R. Kerler ◽  
C. Schuster ◽  
G. Rode ◽  
M. Legner ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dna Repair ◽  
Chemical Carcinogenesis ◽  
Early Stages

scholarly journals DNA repair is activated in early stages of p53-induced apoptosis

2000 ◽  
Vol 7 (4) ◽  
pp. 393-401 ◽  
Author(s):  
F J Geske ◽  
A C Nelson ◽  
R Lieberman ◽  
R Strange ◽  
T Sun ◽  
...  
Keyword(s):  
Dna Repair ◽  
Early Stages ◽  
Induced Apoptosis

scholarly journals Oncogenes - the basics

2018 ◽  
Vol 3 (4) ◽  
pp. 35-37
Author(s):  
Arnab Ghosh ◽  
Diasma Ghartimagar ◽  
Sushma Thapa
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Normal Cell ◽  
Tumor Formation ◽  
Precursor Cell ◽  
Single Precursor ◽  
Normal Cell Cycle

Normal cell cycle and cell proliferation are regulated by several genes which can be broadly classified into 4 groups viz, proto-oncogenes, tumor suppressor genes, genes regulating apoptosis and genes involved in DNA repair. These genes may be defective due to different factors. The defective genes may lead to production of abnormal proteins which may lead to disruption of the normal cell cycle and proliferation. A single precursor cell with defective gene proliferates surpassing the normal physiologic regulatory process and leads to tumor formation, so, traditionally,it is said that “tumors are clonal”.

scholarly journals MicroRNA-146a-5p enhances radiosensitivity in hepatocellular carcinoma through replication protein A3-induced activation of the DNA repair pathway

2019 ◽  
Vol 316 (3) ◽  
pp. C299-C311 ◽  
Author(s):  
Jing Luo ◽  
Zhong-Zhou Si ◽  
Ting Li ◽  
Jie-Qun Li ◽  
Zhong-Qiang Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Dna Repair ◽  
Dna Damage Repair ◽  
Replication Protein ◽  
Repair Pathway ◽  
Related Factors ◽  
Damage Repair ◽  
Hcc Cells

Hepatocellular carcinoma (HCC) is known for its high mortality rate worldwide. Based on intensive studies, microRNA (miRNA) expression functions in tumor suppression. Therefore, we aimed to evaluate the contribution of miR-146a-5p to radiosensitivity in HCC through the activation of the DNA damage repair pathway by binding to replication protein A3 (RPA3). First, the limma package of R was performed to differentially analyze HCC expression chip, and regulative miRNA of RPA3 was predicted. Expression of miR-146a-5p, RPA3, and DNA damage repair pathway-related factors in tissues and cells was determined. The effects of radiotherapy on the expression of miR-146a-5p and RPA3 as well as on cell radiosensitivity, proliferation, cell cycle, and apoptosis were also assessed. The results showed that there exists a close correlation between miR-146a and the radiotherapy effect on HCC progression through regulation of RPA3 and the DNA repair pathway. The positive rate of ATM, pCHK2, and Rad51 in HCC tissues was higher when compared with that of the paracancerous tissues. SMMC-7721 and HepG2 cell proliferation were significantly inhibited following 8 Gy 6Mv dose. MiR-146a-5p restrained the expression of RPA3 and promoted the expression of relative genes associated with the DNA repair pathway. In addition, miR-146a-5p overexpression suppresses cell proliferation and enhances radiosensitivity and cell apoptosis in HCC cells. In conclusion, the present study revealed that miR-146a-5p could lead to the restriction of proliferation and the promotion of radiosensitivity and apoptosis in HCC cells through activation of DNA repair pathway and inhibition of RPA3.

scholarly journals Features of DNA Repair in the Early Stages of Mammalian Embryonic Development

Genes ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1138 ◽  
Author(s):  
Evgenia V. Khokhlova ◽  
Zoia S. Fesenko ◽  
Julia V. Sopova ◽  
Elena I. Leonova
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Embryonic Development ◽  
Somatic Cells ◽  
Genomic Integrity ◽  
Embryonic Period ◽  
Early Stages ◽  
Mammalian Embryos ◽  
Disparate Data ◽  
Mammalian Embryonic Development

Cell repair machinery is responsible for protecting the genome from endogenous and exogenous effects that induce DNA damage. Mutations that occur in somatic cells lead to dysfunction in certain tissues or organs, while a violation of genomic integrity during the embryonic period often leads to death. A mammalian embryo’s ability to respond to damaged DNA and repair it, as well as its sensitivity to specific lesions, is still not well understood. In this review, we combine disparate data on repair processes in the early stages of preimplantation development in mammalian embryos.

scholarly journals BRCT Domain-Containing Protein PTIP Is Essential for Progression through Mitosis

2003 ◽  
Vol 23 (5) ◽  
pp. 1666-1673 ◽  
Author(s):  
Eun Ah Cho ◽  
Marc J. Prindle ◽  
Gregory R. Dressler
Keyword(s):  
Cell Proliferation ◽  
Dna Repair ◽  
Cell Cycle Control ◽  
Embryonic Stem ◽  
Essential Element ◽  
Brct Domain ◽  
Transactivation Domain ◽  
Mouse Development ◽  
Nuclear Condensation ◽  
Interacting Protein

ABSTRACT The Pax transactivation domain-interacting protein (PTIP) is a large nuclear protein with multiple BRCT domains that was identified on the basis of its interaction with transcription factors of the Pax and Smad families. To address the function of PTIP during mouse development, we generated a constitutive null allele. Homozygous PTIP mutants are developmentally retarded, disorganized, and embryonic lethal by day 9.5 of embryonic development (E9.5). PTIP mutant cells appear to replicate DNA but show reduced levels of mitosis and widespread cell death by E8.5. DNA damage appears to precede nuclear condensation at E7.5, suggesting a defect in DNA repair. Neither embryonic fibroblast nor embryonic stem cells from PTIP mutants proliferate in culture, suggesting a fundamental defect in cell proliferation. Trophoblast cells from PTIP mutants are more sensitive to DNA-damaging agents. Condensation of chromatin and expression of phospho-histone H3 are also affected in PTIP mutants, and this may underlie the inability of PTIP mutants to progress through mitosis. Given the role of BRCT domain proteins in DNA repair and cell cycle control, we propose that PTIP is an essential element of the cell proliferation machinery, perhaps by functioning in the DNA repair pathways.

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