UC San Diego

Prostate cancer (PCa) accounts for 3.8% of cancer related deaths in males worldwide.1 Therapeutic and surgical developments have mitigated the mortality of localized prostate cancer, yet upon the progression of the cancer to a metastatic state, the disease becomes quite lethal. New technologies and research targeting prostate cancer aim to ameliorate disease progression by inhibiting localized tumor growth or by preventing metastasis. Recent literature has reported the low-molecular-weight protein tyrosine phosphatase (LMPTP) as a protein involved in the progression of prostate cancer.2, 3 By the complete knockout of LMPTP via CRISPR/Cas9 technology, or the inhibition of LMPTP through our recently developed orally bioavailable compound, we looked to confirm LMPTP as an oncogenic protein using systems that model prostate cancer progression. We confirmed that LMPTP confers cancer-like characteristics to prostate cancer cells in vitro and in vivo. Additionally, through molecular techniques such as Western blotting and immunofluorescence, we explored the intracellular mechanism through which LMPTP promotes cancer progression. We report a potential downstream effector of LMPTP action, and a potential axis through which this effector mediates LMPTP’s oncogenic effects. In conclusion, LMPTP is a promising molecule for further phenotypic and mechanistic exploration and in the long term may reveal to be a druggable target for prostate cancer treatment.