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@article{1613920, author = {Lukasova, Emilie and Rezacova, Martina and Bacikova, Alena and Šebejová, Ludmila and Vavrova, Jirina and Kozubek, Stanislav}, article_location = {HOBOKEN}, article_number = {5}, doi = {http://dx.doi.org/10.1002/2211-5463.12632}, keywords = {apoptosis; ATR inhibitor; Chk1 inhibitor; lamin B receptor; replication stress; senescence}, language = {eng}, issn = {2211-5463}, journal = {FEBS Open Bio}, title = {Distinct cellular responses to replication stress leading to apoptosis or senescence}, url = {http://dx.doi.org/10.1002/2211-5463.12632}, volume = {9}, year = {2019} }
TY - JOUR ID - 1613920 AU - Lukasova, Emilie - Rezacova, Martina - Bacikova, Alena - Šebejová, Ludmila - Vavrova, Jirina - Kozubek, Stanislav PY - 2019 TI - Distinct cellular responses to replication stress leading to apoptosis or senescence JF - FEBS Open Bio VL - 9 IS - 5 SP - 870-890 EP - 870-890 PB - WILEY SN - 22115463 KW - apoptosis KW - ATR inhibitor KW - Chk1 inhibitor KW - lamin B receptor KW - replication stress KW - senescence UR - http://dx.doi.org/10.1002/2211-5463.12632 L2 - http://dx.doi.org/10.1002/2211-5463.12632 N2 - Replication stress (RS) is a major driver of genomic instability and tumorigenesis. Here, we investigated whether RS induced by the nucleotide analog fludarabine and specific kinase inhibitors [e.g. targeting checkpoint kinase 1 (Chk1) or ataxia telangiectasia and Rad3-related (ATR)] led to apoptosis or senescence in four cancer cell lines differing in TP53 mutation status and expression of lamin A/C (LA/C). RS resulted in uneven chromatin condensation in all cell types, as evidenced by the presence of metaphasic chromosomes with unrepaired DNA damage, as well as detection of less condensed chromatin in the same nucleus, frequent ultrafine anaphase bridges, and micronuclei. We observed that responses to these chromatin changes may be distinct in individual cell types, suggesting that expression of lamin A/C and lamin B1 (LB1) may play an important role in the transition of damaged cells to senescence. MCF7 mammary carcinoma cells harboring wild-type p53 (WT-p53) and LA/C responded to RS by transition to senescence with a significant reduction of lamin B receptor and LB1 proteins. In contrast, a lymphoid cancer cell line WSU-NHL (WT-p53) lacking LA/C and expressing low levels of LB1 died after several hours, while lines MEC-1 and SU-DHL-4, both with mutated p53, and SU-DHL-4 with mutations in LA/C, died at different rates by apoptosis. Our results show that, in addition to being influenced by p53 mutation status, the response to RS (apoptosis or senescence) may also be influenced by lamin A/C and LB1 status. ER -
LUKASOVA, Emilie, Martina REZACOVA, Alena BACIKOVA, Ludmila ŠEBEJOVÁ, Jirina VAVROVA a Stanislav KOZUBEK. Distinct cellular responses to replication stress leading to apoptosis or senescence. \textit{FEBS Open Bio}. HOBOKEN: WILEY, 2019, roč.~9, č.~5, s.~870-890. ISSN~2211-5463. Dostupné z: https://dx.doi.org/10.1002/2211-5463.12632.
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