Triple-negative breast cancers (TNBCs) have poor prognosis, and chemotherapy remains the mainstay of therapy because of lack of discovered possible target. MYC were found overexpressed in TNBCs compared with other subtypes and especially in those resistant to chemotherapy, but the inhibition has been challenging to achieve. Recently, the cooperation of PIM1 and MYC was identified involved in cell proliferation, migration and apoptosis of TNBCs, which has been reported in hematological malignancy and prostatic cancer. Inhibition of PIM1 can promote the apoptosis of tumor cells and enhance sensitivity to chemotherapy. Notably, PIM1-null mice develop normally and are fertile, suggesting the side effects can be tolerated. Thus, PIM1 may be a promising target in TNBCs and further investigation, both in vivo and in vitro, needs to be carried out.
Keywords: Apoptosis; Cell cycle regulation; MYC; PIM1; Triple-negative breast cancers (TNBCs).