Author Correction: The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT)

Lu, Robert; O'Rourke, Julienne J; Sobinoff, Alexander P.; Allen, Joshua A. M.; Nelson, Christopher B.; Tomlinson, Christopher G.; Lee, Michael; Reddel, Roger R.; Deans, Andrew J.; Pickett, Hilda A.

doi:10.1038/s41467-019-13097-2

Cited by 2 publications

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“…ALT activity has been shown to be associated with elevated levels of telomeric DNA damage and repair, an essential feature of TMM. At the same time, excessive levels of telomeric DNA repair are highly deleterious to ALT cells 54 . In these premises, downregulation of DNA repair proteins by overexpression of miR-708 in ALT cells may serve to prevent excessively elevated levels of DNA repair.…”

Section: Discussionmentioning

confidence: 99%

Functional characterization of miR-708 microRNA in telomerase positive and negative human cancer cells

Kaul

Cheung

Bhargava

et al. 2021

Sci Rep

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Activation of a telomere length maintenance mechanism (TMM), including telomerase and alternative lengthening of telomeres (ALT), is essential for replicative immortality of tumor cells, although its regulatory mechanisms are incompletely understood. We conducted a microRNA (miRNA) microarray analysis on isogenic telomerase positive (TEP) and ALT cancer cell lines. Amongst nine miRNAs that showed difference in their expression in TEP and ALT cancer cells in array analysis, miR-708 was selected for further analysis since it was consistently highly expressed in a large panel of ALT cells. miR-708 in TEP and ALT cancer cells was not correlated with C-circle levels, an established feature of ALT cells. Its overexpression induced suppression of cell migration, invasion, and angiogenesis in both TEP and ALT cells, although cell proliferation was inhibited only in TEP cells suggesting that ALT cells may have acquired the ability to escape inhibition of cell proliferation by sustained miR-708 overexpression. Further, cell proliferation regulation in TEP cells by miR708 appears to be through the CARF-p53 pathway. We demonstrate here that miR-708 (i) is the first miRNA shown to be differentially regulated in TEP and ALT cancer cells, (ii) possesses tumor suppressor function, and (iii) deregulates CARF and p21WAF1-mediated signaling to limit proliferation in TEP cells.

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Section: Discussionmentioning

confidence: 99%