scholarly journals Diallyl Sulfide-Mediated Modulation of the Fatty Acid Synthase (FASN) Leads to Cancer Cell Death in BaP-Induced Lung Carcinogenesis in Swiss Mice

2020 ◽  
Vol Volume 13 ◽  
pp. 1075-1087
Author(s):  
Arif Khan ◽  
Fahad A Alhumaydhi ◽  
Ameen SS Alwashmi ◽  
Khaled S Allemailem ◽  
Mohammed A Alsahli ◽  
...  
Keyword(s):  
Cell Death ◽  
Fatty Acid ◽  
Cancer Cell ◽  
Fatty Acid Synthase ◽  
Lung Carcinogenesis ◽  
Diallyl Sulfide ◽  
Swiss Mice ◽  
Cancer Cell Death

scholarly journals Fatty acid synthase inhibition engages a novel caspase-2 regulatory mechanism to induce ovarian cancer cell death

Oncogene ◽  
2014 ◽  
Vol 34 (25) ◽  
pp. 3264-3272 ◽  
Author(s):  
C-S Yang ◽  
K Matsuura ◽  
N-J Huang ◽  
A C Robeson ◽  
B Huang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Fatty Acid ◽  
Cancer Cell ◽  
Fatty Acid Synthase ◽  
Regulatory Mechanism ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Death ◽  
Caspase 2

scholarly journals Fatty acid synthase inhibition: Metabolic reprogramming leading to cancer cell death

2016 ◽  
Vol 1857 ◽  
pp. e116
Author(s):  
Nastasia Wilfinger ◽  
Kristina Kührer ◽  
Magdalena Billerhart ◽  
Karin Nowikovsky
Keyword(s):  
Cell Death ◽  
Fatty Acid ◽  
Cancer Cell ◽  
Fatty Acid Synthase ◽  
Metabolic Reprogramming ◽  
Cancer Cell Death

scholarly journals Fatty acid synthase (FASN) regulates the mitochondrial priming of cancer cells

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Barbara Schroeder ◽  
Travis Vander Steen ◽  
Ingrid Espinoza ◽  
Chandra M. Kurapaty Venkatapoorna ◽  
Zeng Hu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Fatty Acid Synthase ◽  
Xenograft Model ◽  
Fine Tuning ◽  
Bh3 Mimetic

AbstractInhibitors of the lipogenic enzyme fatty acid synthase (FASN) have attracted much attention in the last decade as potential targeted cancer therapies. However, little is known about the molecular determinants of cancer cell sensitivity to FASN inhibitors (FASNis), which is a major roadblock to their therapeutic application. Here, we find that pharmacological starvation of endogenously produced FAs is a previously unrecognized metabolic stress that heightens mitochondrial apoptotic priming and favors cell death induction by BH3 mimetic inhibitors. Evaluation of the death decision circuits controlled by the BCL-2 family of proteins revealed that FASN inhibition is accompanied by the upregulation of the pro-death BH3-only proteins BIM, PUMA, and NOXA. Cell death triggered by FASN inhibition, which causally involves a palmitate/NADPH-related redox imbalance, is markedly diminished by concurrent loss of BIM or PUMA, suggesting that FASN activity controls cancer cell survival by fine-tuning the BH3 only proteins-dependent mitochondrial threshold for apoptosis. FASN inhibition results in a heightened mitochondrial apoptosis priming, shifting cells toward a primed-for-death state “addicted” to the anti-apoptotic protein BCL-2. Accordingly, co-administration of a FASNi synergistically augments the apoptosis-inducing activity of the dual BCL-XL/BCL-2 inhibitor ABT-263 (navitoclax) and the BCL-2 specific BH3-mimetic ABT-199 (venetoclax). FASN inhibition, however, fails to sensitize breast cancer cells to MCL-1- and BCL-XL-selective inhibitors such as S63845 and A1331852. A human breast cancer xenograft model evidenced that oral administration of the only clinically available FASNi drastically sensitizes FASN-addicted breast tumors to ineffective single-agents navitoclax and venetoclax in vivo. In summary, a novel FASN-driven facet of the mitochondrial priming mechanistically links the redox-buffering mechanism of FASN activity to the intrinsic apoptotic threshold in breast cancer cells. Combining next-generation FASNis with BCL-2-specific BH3 mimetics that directly activate the apoptotic machinery might generate more potent and longer-lasting antitumor responses in a clinical setting.

New Insight into 2-Methoxyestradiol- a Possible Physiological Link between Neurodegeneration and Cancer Cell Death

2016 ◽  
Vol 23 (15) ◽  
pp. 1513-1527 ◽  
Author(s):  
Magdalena Gorska ◽  
Alicja Kuban-Jankowska ◽  
Jaroslaw Slawek ◽  
Michal Wozniak
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Cancer Cell Death ◽  
Insight Into

Zinc chelator TPEN induces pancreatic cancer cell death through causing oxidative stress and inhibiting cell autophagy

2019 ◽  
Vol 234 (11) ◽  
pp. 20648-20661 ◽  
Author(s):  
Zhen Yu ◽  
Ze Yu ◽  
ZhenBao Chen ◽  
Lin Yang ◽  
MingJun Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Death ◽  
Zinc Chelator

Magneto Mitochondrial Dysfunction Mediated Cancer Cell Death Using Intracellular Magnetic Nano-Transducers

2021 ◽  
Author(s):  
Wooram Park ◽  
Seok-Jo Kim ◽  
Paul Cheresh ◽  
Jeanho Yun ◽  
Byeongdu Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Cancer Cell ◽  
High Sensitivity ◽  
Intrinsic Pathway ◽  
Cancer Cell Death

Mitochondria are crucial regulators of the intrinsic pathway of cancer cell death. The high sensitivity of cancer cells to mitochondrial dysfunction offers opportunities for emerging targets in cancer therapy. Herein,...

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