Livin participates in resistance to trastuzumab therapy for breast cancer through ERK1/2 and AKT pathways and promotes EMT-like phenotype.

Remarkably, our finding that livin confers resistance to trastuzumab is strongly supported by clinical data that patients with livin-overexpressing tumors did not respond to trastuzumab as well as those with normal livin, and the difference was statistically highly significant ( p < 0.01), even in the small cohort.

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Moreover, the expression of livin was further upregulated after trastuzumab therapy in both resistant and sensitive tumors, but the difference did not reach statistical significance ( Fig. 7A–C ), which implies that, given a prolonged period of treatment with trastuzumab, acquired trastuzumab resistance due to the induction of livin may occur.

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