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MiR-502 is the first reported miRNA simultaneously targeting two components of the classical non-homologous end joining (C-NHEJ) in pancreatic cell lines.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers. Acquired inherited and/or somatic mutations drive its development. In order to prevent the formation of these mutations, precise and immediate repair of any DNA damage is indispensable. Non-homologous end-joining (NHEJ) is the key mechanism of DNA double-strand break repair. Here, we report that miR-502 targets two components in pancreatic cell lines, Ku70 and XLF of the C-NHEJ. Interestingly, we also observed an attenuated cell cycle response to gamma ionizing radiation (?-IR) via diminished phosphorylation of checkpoint kinase 1 (Chk1) on serine 345 in these cell lines. Altogether, pancreatic cells showed increased susceptibility to ?-IR via direct inhibition of DNA double-strand break repair and attenuation of the cell cycle response.

SUBMITTER: Smolinska A

PROVIDER: S-EPMC7002776 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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MiR-502 is the first reported miRNA simultaneously targeting two components of the classical non-homologous end joining (C-NHEJ) in pancreatic cell lines.

Smolinska Agnieszka A Swoboda Julia J Fendler Wojciech W Lerch Markus M MM Sendler Matthias M Moskwa Patryk P

Heliyon 20200118 1

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers. Acquired inherited and/or somatic mutations drive its development. In order to prevent the formation of these mutations, precise and immediate repair of any DNA damage is indispensable. Non-homologous end-joining (NHEJ) is the key mechanism of DNA double-strand break repair. Here, we report that miR-502 targets two components in pancreatic cell lines, Ku70 and XLF of the C-NHEJ. Interestingly, we also observed an attenuated ...[more]

PMID: 32042960

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