Efficacy of biologic agents (BA) in metastatic, triple-negative breast cancer (TNBC): A systematic review.

Verde, Nicla Maria La; Bramati, Annalisa; Bianchi, Antonio; Galfrascoli, Elena; Sburlati, P.; Garassino, Marina Chiara; Piva, Sheila; Torri, V.; Cinquini, Michela; Farina, G.

doi:10.1200/jco.2011.29.15_suppl.e11587

Cited by 2 publications

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“…Triple-negative breast cancer (TNBC) cells exhibit a high metastatic potential and lack of standard pharmacologic therapy 5 , 7 , affecting the overall survival of women with this breast cancer sub-type 54 . These considerations highlight the need to understand the biology of TNBC cells and to search for novel targets for anti-cancer therapies.…”

Section: Discussionmentioning

confidence: 99%

FR58P1a; a new uncoupler of OXPHOS that inhibits migration in triple-negative breast cancer cells via Sirt1/AMPK/β1-integrin pathway

Urra

Muñoz

Córdova-Delgado

et al. 2018

Sci Rep

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Highly malignant triple-negative breast cancer (TNBC) cells rely mostly on glycolysis to maintain cellular homeostasis; however, mitochondria are still required for migration and metastasis. Taking advantage of the metabolic flexibility of TNBC MDA-MB-231 cells to generate subpopulations with glycolytic or oxidative phenotypes, we screened phenolic compounds containing an ortho-carbonyl group with mitochondrial activity and identified a bromoalkyl-ester of hydroquinone named FR58P1a, as a mitochondrial metabolism-affecting compound that uncouples OXPHOS through a protonophoric mechanism. In contrast to well-known protonophore uncoupler FCCP, FR58P1a does not depolarize the plasma membrane and its effect on the mitochondrial membrane potential and bioenergetics is moderate suggesting a mild uncoupling of OXPHOS. FR58P1a activates AMPK in a Sirt1-dependent fashion. Although the activation of Sirt1/AMPK axis by FR58P1a has a cyto-protective role, selectively inhibits fibronectin-dependent adhesion and migration in TNBC cells but not in non-tumoral MCF10A cells by decreasing β1-integrin at the cell surface. Prolonged exposure to FR58P1a triggers a metabolic reprograming in TNBC cells characterized by down-regulation of OXPHOS-related genes that promote cell survival but comprise their ability to migrate. Taken together, our results show that TNBC cell migration is susceptible to mitochondrial alterations induced by small molecules as FR58P1a, which may have therapeutic implications.

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Section: Discussionmentioning

confidence: 99%

FR58P1a; a new uncoupler of OXPHOS that inhibits migration in triple-negative breast cancer cells via Sirt1/AMPK/β1-integrin pathway

Urra

Muñoz

Córdova-Delgado

et al. 2018

Sci Rep

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Critical issues on high-dose chemotherapy with autologous hematopoietic progenitor cell transplantation in breast cancer patients

Martino

Bottini

Rosti

et al. 2012

Expert Opinion on Biological Therapy

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HDC with AHPCT has become a safe treatment modality and an advantage in disease-free survival has been observed in most of the studies with HDC, with the caveat that today, even a limited relapse-free survival and progression-free survival benefit is sufficient for the approval of new antineoplastic agents. Moreover, in HRBC, an overall survival benefit by HDC could be achieved in the HER2-ve and triple-negative populations and, in this setting, HDC with AHPCT represents a therapeutic option that can be proposed to well-informed patients. In MBC, the HDC approach should be investigated further in selected patients with HER2-ve, chemosensitive disease. This paper is not intended to give any conclusion, but rather to open a debate on the value of HDC in HR and MBC.

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Efficacy of biologic agents (BA) in metastatic, triple-negative breast cancer (TNBC): A systematic review.

Cited by 2 publications

References 0 publications

FR58P1a; a new uncoupler of OXPHOS that inhibits migration in triple-negative breast cancer cells via Sirt1/AMPK/β1-integrin pathway

FR58P1a; a new uncoupler of OXPHOS that inhibits migration in triple-negative breast cancer cells via Sirt1/AMPK/β1-integrin pathway

Critical issues on high-dose chemotherapy with autologous hematopoietic progenitor cell transplantation in breast cancer patients

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