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. Author manuscript; available in PMC: 2018 May 10.
Published in final edited form as: Cell Death Differ. 2017 Dec 11;25(5):935–950. doi: 10.1038/s41418-017-0030-2

Figure 8.

Figure 8

Working model depicting proposed LOXL3 roles in melanoma. Melanoma arises through the progressive accumulation of genomic alterations resulting in uncontrolled tumor cell proliferation followed by invasion and metastasis. High levels of LOXL3 (A) would sustain effective DNA repair and activation of cell-cycle checkpoint pathways allowing melanoma cells to deal with DNA damage. LOXL3 targeting (B) would hamper the activation of a competent DNA damage checkpoint leading to a halt in cell proliferation and abnormal mitosis. The increase in genomic instability due to DSBs and mitotic catastrophes would ultimately lead to apoptosis of melanoma cells.