Figure 9. Model to explain the role of NUCKS1 in tumor initiation and progression.

a, b. Partial deficiency of NUCKS1 leads to a defect in DNA double-strand break (DSB) repair and to genome rearrangements (i.e., translocations) after ionizing radiation (IR) exposure. c. Tumor initiating cells experience increased replication stress, as described previously [60–62], which potentially may be ameliorated by up-regulation of NUCKS1 expression. d. High levels of NUCKS1 provide a selective advantage and promote TL growth, and e. invasion of the tumor border leading to f. intravasation of TL cells into the circulatory system.