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GLS2 is protumorigenic in breast cancers
Marilia M Dias1,2, Douglas Adamoski1,2, Larissa M Dos Reis1,2
1Brazilian Biosciences National Laboratory (LNBio), Brazilian Center for Research in Energy and Materials (CNPEM), Campinas, Sao Paulo, 13083-970, Brazil.
Oncogene
|September 22, 2019
Summary
Glutaminase 2 (GLS2) unexpectedly promotes triple-negative breast cancer growth and metastasis, challenging its tumor-suppressive role. Targeting GLS2 may offer a new therapeutic strategy for this aggressive cancer.
Area of Science:
- Oncology
- Cancer Metabolism
- Molecular Biology
Background:
- Cancer cells rely on glutamine metabolism for survival, often involving glutaminase 1 (GLS).
- GLS2 typically exhibits tumor-suppressive functions, contrasting with GLS1's oncogenic roles.
- Triple-negative breast cancer (TNBC) shows high GLS levels and dependence on glutamine, but also expresses GLS2.
Purpose of the Study:
- To investigate the role of GLS2 in triple-negative breast cancer (TNBC).
- To determine if GLS2 acts as a tumor suppressor or promoter in TNBC.
- To explore GLS2 as a potential therapeutic target in breast cancer.
Main Methods:
- Utilized GLS inhibitors (CB-839, BPTES) and GLS knockdown in breast cancer cell lines.
- Assessed cell proliferation, TCA cycle activity, redox balance, and mitochondrial function.
- Examined GLS2 expression, cell migration, invasion, mesenchymal markers, and in vivo metastasis.
Main Results:
- Endogenous GLS2 expression rescued proliferation and metabolic functions after GLS inhibition.
- GLS2 knockdown reduced cell proliferation and glutamine metabolism.
- Drug-resistant TNBC cells showed increased GLS2, enhanced migration, invasion, and metastasis.
- GLS2 amplification/overexpression correlated with worse patient survival outcomes.
Conclusions:
- GLS2 unexpectedly promotes proliferation and metastasis in breast cancer, particularly TNBC.
- GLS2's role is contrary to its established tumor-suppressive function.
- GLS2 represents a novel therapeutic target for breast cancer treatment.
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