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PIM1: a promising target in patients with triple-negative breast cancer
Wen Zhao1, RuiYue Qiu1, Pan Li1
1Department of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061, Shaanxi, People's Republic of China.
Abstract:
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.
Insights
Triple-negative breast cancer (TNBC) shows poor prognosis. Targeting PIM1 kinase, in cooperation with MYC, may enhance chemotherapy sensitivity and tumor cell apoptosis in TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Triple-negative breast cancer (TNBC) presents a poor prognosis with limited therapeutic targets.
- Chemotherapy is the primary treatment, but resistance is a significant challenge.
- MYC oncoprotein is overexpressed in TNBC, particularly in chemotherapy-resistant cases, yet direct inhibition is difficult.
Purpose of the Study:
- To investigate the role of PIM1 kinase in TNBC proliferation, migration, and apoptosis.
- To evaluate PIM1 as a potential therapeutic target in TNBC, especially in conjunction with MYC.
- To assess the feasibility of PIM1 inhibition for enhancing chemotherapy sensitivity.
Main Methods:
- Analysis of MYC and PIM1 expression in TNBC subtypes.
- Investigating the cooperative effects of PIM1 and MYC on TNBC cell behavior.
- Evaluating the impact of PIM1 inhibition on tumor cell apoptosis and chemotherapy response.
- Assessing potential side effects using PIM1-null mouse models.
Main Results:
- PIM1 and MYC cooperate in regulating TNBC cell proliferation, migration, and apoptosis.
- Inhibition of PIM1 promotes tumor cell apoptosis and sensitizes TNBC to chemotherapy.
- PIM1-null mice exhibit normal development and fertility, indicating tolerable side effects.
Conclusions:
- PIM1 kinase is a promising therapeutic target for TNBC.
- Targeting PIM1, in combination with MYC, offers a potential strategy to overcome chemotherapy resistance.
- Further in vivo and in vitro studies are warranted to validate PIM1 as a therapeutic target for TNBC.
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