Metabolic reprogramming in triple-negative breast cancer DOI Creative Commons
Zhanyu Wang,

Qianjin Jiang,

Chenfang Dong

и другие.

Cancer Biology and Medicine, Год журнала: 2020, Номер 17(1), С. 44 - 59

Опубликована: Янв. 1, 2020

Since triple-negative breast cancer (TNBC) was first defined over a decade ago, increasing studies have focused on its genetic and molecular characteristics. Patients diagnosed with TNBC, compared to those other subtypes, relatively poor outcomes due high tumor aggressiveness lack of targeted treatment. Metabolic reprogramming, an emerging hallmark cancer, is hijacked by TNBC fulfill bioenergetic biosynthetic demands; maintain the redox balance; further promote oncogenic signaling, cell proliferation, metastasis. Understanding mechanisms metabolic remodeling may guide design strategies for effective intervention TNBC. Here, we review reprogramming glycolysis, oxidative phosphorylation, amino acid metabolism, lipid branched pathways in explore opportunities new biomarkers, imaging modalities, metabolically therapies.

Язык: Английский

SLC transporters: structure, function, and drug discovery DOI
Claire Colas, Peter M.U. Ung, Avner Schlessinger

и другие.

MedChemComm, Год журнала: 2016, Номер 7(6), С. 1069 - 1081

Опубликована: Янв. 1, 2016

The human solute carrier (SLC) transporters are important targets for drug development.

Язык: Английский

Процитировано

182
Genetic Ablation of the Cystine Transporter xCT in PDAC Cells Inhibits mTORC1, Growth, Survival, and Tumor Formation via Nutrient and Oxidative Stresses DOI
Boutaina Daher, Scott K. Parks, Jérôme Durivault

и другие.

Cancer Research, Год журнала: 2019, Номер 79(15), С. 3877 - 3890

Опубликована: Июнь 7, 2019

Although chemoresistance remains a primary challenge in the treatment of pancreatic ductal adenocarcinoma (PDAC), exploiting oxidative stress might offer novel therapeutic clues. Here we explored potential targeting cystine/glutamate exchanger (SLC7A11/xCT), which contributes to maintenance intracellular glutathione (GSH). Genomic disruption xCT via CRISPR-Cas9 was achieved two PDAC cell lines, MiaPaCa-2 and Capan-2, xCT-KO clones were cultivated presence N-acetylcysteine. several cystine/cysteine transporters have been identified, our findings demonstrate that, vitro, plays major role cysteine balance GSH biosynthesis. As consequence, both lines exhibited amino acid with activation GCN2 subsequent induction ATF4, inhibition mTORC1, proliferation arrest, death. Tumor xenograft growth delayed but not suppressed cells, indicated key also additional mechanisms for homeostasis vivo. Moreover, rapid depletion cells led accumulation lipid peroxides swelling. These hallmarks ferroptotic death prevented by vitamin E or iron chelation. Finally, vitro pharmacologic low concentrations erastin phenocopied potentiated cytotoxic effects gemcitabine cisplatin lines. In conclusion, strongly support that xCT, its dual nutritional cellular stresses, has great as an anticancer strategy. SIGNIFICANCE: The is essential redox therapy inducing ferroptosis.

Язык: Английский

Процитировано

180
Metabolic Reprogramming in Triple-Negative Breast Cancer DOI Creative Commons
Xiangyu Sun, Mozhi Wang, Mengshen Wang

и другие.

Frontiers in Oncology, Год журнала: 2020, Номер 10

Опубликована: Март 31, 2020

Metabolic reprogramming is an emerging hallmark of cancer cells, in which cells exhibit distinct metabolic phenotypes to fuel their proliferation and progression. The significant advancements made the area make possible new strategies for overcoming malignant cancer, including triple-negative breast cancer. Triple-negative associated with high histologic grade, aggressive phenotype, poor prognosis. Even though patients benefit from standard chemotherapy, they still face recurrence rates are more likely develop resistance chemotherapeutic drugs. Therefore, there urgent need explore vulnerabilities novel therapeutic drugs improve clinical outcomes patients. may provide promising targets treatment In this paper, we primarily discuss how reprogram phenotype that stromal microenvironment survive under nutrient-poor conditions. Considering metastasis chemoresistance main contributors mortality patients, also focus on role adaption mediating tumors.

Язык: Английский

Процитировано

170
STAT proteins in cancer: orchestration of metabolism DOI
Yijia Li, Chunyan Zhang, Antons Martincuks

и другие.

Nature reviews. Cancer, Год журнала: 2023, Номер 23(3), С. 115 - 134

Опубликована: Янв. 3, 2023

Язык: Английский

Процитировано

162
Metabolic reprogramming in triple-negative breast cancer DOI Creative Commons
Zhanyu Wang,

Qianjin Jiang,

Chenfang Dong

и другие.

Cancer Biology and Medicine, Год журнала: 2020, Номер 17(1), С. 44 - 59

Опубликована: Янв. 1, 2020

Since triple-negative breast cancer (TNBC) was first defined over a decade ago, increasing studies have focused on its genetic and molecular characteristics. Patients diagnosed with TNBC, compared to those other subtypes, relatively poor outcomes due high tumor aggressiveness lack of targeted treatment. Metabolic reprogramming, an emerging hallmark cancer, is hijacked by TNBC fulfill bioenergetic biosynthetic demands; maintain the redox balance; further promote oncogenic signaling, cell proliferation, metastasis. Understanding mechanisms metabolic remodeling may guide design strategies for effective intervention TNBC. Here, we review reprogramming glycolysis, oxidative phosphorylation, amino acid metabolism, lipid branched pathways in explore opportunities new biomarkers, imaging modalities, metabolically therapies.

Язык: Английский

Процитировано

142