Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast neoplasms with a higher risk of recurrence and metastasis than non-TNBC. Nevertheless, the factors responsible for the differences in the malignant behavior between TNBC and non-TNBC are not fully explored. Proline rich 15 (PRR15) is a protein involved in the progression of several tumor types, but its mechanisms are still controversial. Therefore, this study aimed to investigate the biological role and clinical applications of PRR15 on TNBC. PRR15 gene was differentially expressed between TNBC and non-TNBC patients, previously described as an oncogenic factor in breast cancer. However, our results showed a decreased expression of PRR15 that portended a favorable prognosis in TNBC rather than non-TNBC. PRR15 knockdown facilitated the proliferation, migration, and invasive ability of TNBC cells in vitro and in vivo, which was abolished by PRR15 restoration, without remarkable effects on non-TNBC. High-throughput drug sensitivity revealed that PI3K/Akt signaling was involved in the aggressive properties of PRR15 silencing, which was confirmed by the PI3K/Akt signaling activation in the tumors of PRR15Low patients, and PI3K inhibitor reversed the metastatic capacity of TNBC in mice. The reduced PRR15 expression in TNBC patients was positively correlated with more aggressive clinicopathological characteristics, enhanced metastasis, and poor disease-free survival. Collectively, PRR15 down-regulation promotes malignant progression through the PI3K/Akt signaling in TNBC rather than in non-TNBC, affects the response of TNBC cells to antitumor agents, and is a promising indicator of disease outcomes in TNBC.
Prostate cancer (PCa) is the most frequent cancer of the male genitourinary system and the second most common cancer in men worldwide. PCa has become one of the leading diseases endangering men's health in Asia in recent years, with a large increase in morbidity and mortality. MTA1 (metastasis-associated antigen-1), a transcriptional coregulator involved in histone deacetylation and nucleosome remodeling, is a member of the MTA family. MTA1 is involved in cell signaling, chromosomal remodeling, and transcriptional activities, all of which are important for epithelial cell progression, invasion, and growth. MTA1 has been demonstrated to play a significant role in the formation, progression, and metastasis of PCa, and MTA1 expression is specifically linked to PCa bone metastases. Therefore, MTA1 may be a potential target for PCa prevention and treatment. Here, we reviewed the structure, function, and expression of MTA1 in PCa as well as drugs that target MTA1 to highlight a potential new treatment for PCa.
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