scholarly journals Balancing biosynthesis and bioenergetics: metabolic programs in oncogenesis

2010 ◽  
Vol 17 (4) ◽  
pp. R287-R304 ◽  
Author(s):  
Jennifer F Barger ◽  
David R Plas
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Signal Transduction Pathway ◽  
Building Blocks ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Pathway Activation ◽  
Cancer Cell Metabolism ◽  
Programed Cell Death

Cancer biologists' search for new chemotherapy targets is reinvigorating the study of how cancer cell metabolism determines both oncogenic potential and chemotherapeutic responses. Oncogenic metabolic programs support the bioenergetics associated with resistance to programed cell death and provide biosynthetic building blocks for cell growth and mitogenesis. Both signal transduction pathway activation and direct mutations in key metabolic enzymes can activate the metabolic programs that support cancer cell growth. Cancer-associated metabolic programs include glycolysis, glutamine oxidation, and fatty acid metabolism. Recent observations are revealing the regulatory mechanisms that activate cancer-associated metabolism, and the competitive advantages provided to transformed cells by their metabolic programs. In this study, we review recent results illustrating the mechanisms and functional impact of each of these oncogenic metabolic programs in cancer cell growth and survival.

scholarly journals Novel Polyphenols That Inhibit Colon Cancer Cell Growth Affecting Cancer Cell Metabolism

2018 ◽  
Vol 366 (2) ◽  
pp. 377-389 ◽  
Author(s):  
Marta Gómez de Cedrón ◽  
Teodoro Vargas ◽  
Andrés Madrona ◽  
Aranza Jiménez ◽  
María-Jesús Pérez-Pérez ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Colon Cancer Cell ◽  
Cancer Cell Growth ◽  
Cancer Cell Metabolism

scholarly journals Estrogen-induced epigenetic silencing of FTH1 and TFRC genes reduces liver cancer cell growth and survival

Epigenetics ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. 1302-1318
Author(s):  
Jibran Sualeh Muhammad ◽  
Khuloud Bajbouj ◽  
Jasmin Shafarin ◽  
Mawieh Hamad
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Epigenetic Silencing ◽  
Liver Cancer Cell ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Cell Growth And Survival

scholarly journals Bone matrix osteonectin limits prostate cancer cell growth and survival

2012 ◽  
Vol 31 (5) ◽  
pp. 299-307 ◽  
Author(s):  
Kristina Kapinas ◽  
Katie M. Lowther ◽  
Catherine B. Kessler ◽  
Karissa Tilbury ◽  
Jay R. Lieberman ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Bone Matrix ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Cell Growth And Survival

scholarly journals Follistatin-like protein 1 sustains colon cancer cell growth and survival

Oncotarget ◽  
2018 ◽  
Vol 9 (58) ◽  
pp. 31278-31290 ◽  
Author(s):  
Gerolamo Bevivino ◽  
Silvia Sedda ◽  
Eleonora Franzè ◽  
Carmine Stolfi ◽  
Antonio Di Grazia ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Cell Growth And Survival

scholarly journals Estrogen-induced hypomethylation and overexpression of YAP1 facilitate breast cancer cell growth and survival

Neoplasia ◽  
2021 ◽  
Vol 23 (1) ◽  
pp. 68-79
Author(s):  
Jibran Sualeh Muhammad ◽  
Maha Guimei ◽  
Manju Nidagodu Jayakumar ◽  
Jasmin Shafarin ◽  
Aisha Saleh Janeeh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Breast Cancer Cell Growth ◽  
Cell Growth And Survival

scholarly journals Mitochondrial VDAC1 Silencing Leads to Metabolic Rewiring and the Reprogramming of Tumour Cells into Advanced Differentiated States

Cancers ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 499 ◽  
Author(s):  
Tasleem Arif ◽  
Avijit Paul ◽  
Yakov Krelin ◽  
Anna Shteinfer-Kuzmine ◽  
Varda Shoshan-Barmatz
Keyword(s):  
Lung Cancer ◽  
Cell Differentiation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Tumour Growth ◽  
Cell Metabolism ◽  
Metabolic Reprogramming ◽  
Residual Tumour ◽  
Cancer Cell Metabolism

Oncogenic properties, along with the metabolic reprogramming necessary for tumour growth and motility, are acquired by cancer cells. Thus, tumour metabolism is becoming a target for cancer therapy. Here, cancer cell metabolism was tackled by silencing the expression of voltage-dependent anion channel 1 (VDAC1), a mitochondrial protein that controls cell energy, as well as metabolic and survival pathways and that is often over-expressed in many cancers. We demonstrated that silencing VDAC1 expression using human-specific siRNA (si-hVDAC1) inhibited cancer cell growth, both in vitro and in mouse xenograft models of human glioblastoma (U-87MG), lung cancer (A549), and triple negative breast cancer (MDA-MB-231). Importantly, treatment with si-hVDAC1 induced metabolic rewiring of the cancer cells, reversing their oncogenic properties and diverting them towards differentiated-like cells. The si-hVDAC1-treated residual “tumour” showed reprogrammed metabolism, decreased proliferation, inhibited stemness and altered expression of genes and proteins, leading to cell differentiation toward less malignant lineages. These VDAC1 depletion-mediated effects involved alterations in master transcription factors associated with cancer hallmarks, such as highly increased expression of p53 and decreased expression of HIF-1a and c-Myc that regulate signalling pathways (e.g., AMPK, mTOR). High expression of p53 and the pro-apoptotic proteins cytochrome c and caspases without induction of apoptosis points to functions for these proteins in promoting cell differentiation. These results clearly show that VDAC1 depletion similarly leads to a rewiring of cancer cell metabolism in breast and lung cancer and glioblastoma, regardless of origin or mutational status. This metabolic reprogramming results in cell growth arrest and inhibited tumour growth while encouraging cell differentiation, thus generating cells with decreased proliferation capacity. These results further suggest VDAC1 to be an innovative and markedly potent therapeutic target.

scholarly journals Lipophilic statins limit cancer cell growth and survival, via involvement of Akt signaling

PLoS ONE ◽  
2018 ◽  
Vol 13 (5) ◽  
pp. e0197422 ◽  
Author(s):  
Colin H. Beckwitt ◽  
Keisuke Shiraha ◽  
Alan Wells
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Akt Signaling ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Cell Growth And Survival

scholarly journals SLC1A5 Mediates Glutamine Transport Required for Lung Cancer Cell Growth and Survival

2012 ◽  
Vol 19 (3) ◽  
pp. 560-570 ◽  
Author(s):  
Mohamed Hassanein ◽  
Megan D. Hoeksema ◽  
Masakazu Shiota ◽  
Jun Qian ◽  
Bradford K. Harris ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Glutamine Transport ◽  
Cell Growth And Survival
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