scholarly journals Mitochondrial metabolic alterations in cancer cells and related therapeutic targets

2020 ◽  
Vol 98 ◽  
pp. 1-3
Author(s):  
Chiara Riganti ◽  
Massimo Donadelli
Keyword(s):  
Cancer Cells ◽  
Therapeutic Targets ◽  
Metabolic Alterations

scholarly journals Regulation of Metabolic Reprogramming by Long Non-Coding RNAs in Cancer

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3485
Author(s):  
Assunta Sellitto ◽  
Giovanni Pecoraro ◽  
Giorgio Giurato ◽  
Giovanni Nassa ◽  
Francesca Rizzo ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Cancer Cells ◽  
Metabolic Reprogramming ◽  
Metabolic Phenotype ◽  
Metabolic Alterations ◽  
Cell Proliferation And Differentiation ◽  
Non Coding Rna ◽  
Proliferation And Differentiation ◽  
Non Coding Rnas ◽  
Additional Level

Metabolic reprogramming is a well described hallmark of cancer. Oncogenic stimuli and the microenvironment shape the metabolic phenotype of cancer cells, causing pathological modifications of carbohydrate, amino acid and lipid metabolism that support the uncontrolled growth and proliferation of cancer cells. Conversely, metabolic alterations in cancer can drive changes in genetic programs affecting cell proliferation and differentiation. In recent years, the role of non-coding RNAs in metabolic reprogramming in cancer has been extensively studied. Here, we review this topic, with a focus on glucose, glutamine, and lipid metabolism and point to some evidence that metabolic alterations occurring in cancer can drive changes in non-coding RNA expression, thus adding an additional level of complexity in the relationship between metabolism and genetic programs in cancer cells.

scholarly journals Proteotranscriptomic Profiling of 231-BR Breast Cancer Cells: Identification of Potential Biomarkers and Therapeutic Targets for Brain Metastasis

2015 ◽  
Vol 14 (9) ◽  
pp. 2316-2330 ◽  
Author(s):  
Matthew D. Dun ◽  
Robert J. Chalkley ◽  
Sam Faulkner ◽  
Sheridan Keene ◽  
Kelly A. Avery-Kiejda ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Brain Metastasis ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Targets ◽  
Potential Biomarkers

scholarly journals Therapeutic Targeting of Epithelial Plasticity Programs: Focus on the Epithelial-Mesenchymal Transition

2017 ◽  
Vol 203 (2) ◽  
pp. 114-127 ◽  
Author(s):  
Reem Malek ◽  
Hailun Wang ◽  
Kekoa Taparra ◽  
Phuoc T. Tran
Keyword(s):  
Cancer Cells ◽  
Regulatory Networks ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Therapeutic Targets ◽  
Treatment Resistance ◽  
Mesenchymal Transition ◽  
Epithelial Plasticity ◽  
Canonical Pathways

Mounting data points to epithelial plasticity programs such as the epithelial-mesenchymal transition (EMT) as clinically relevant therapeutic targets for the treatment of malignant tumors. In addition to the widely realized role of EMT in increasing cancer cell invasiveness during cancer metastasis, the EMT has also been implicated in allowing cancer cells to avoid tumor suppressor pathways during early tumorigenesis. In addition, data linking EMT to innate and acquired treatment resistance further points towards the desire to develop pharmacological therapies to target epithelial plasticity in cancer. In this review we organized our discussion on pathways and agents that can be used to target the EMT in cancer into 3 groups: (1) extracellular inducers of EMT, (2) the transcription factors that orchestrate the EMT transcriptome, and (3) the downstream effectors of EMT. We highlight only briefly specific canonical pathways known to be involved in EMT, such as the signal transduction pathways TGFβ, EFGR, and Axl-Gas6. We emphasize in more detail pathways that we believe are emerging novel pathways and therapeutic targets such as epigenetic therapies, glycosylation pathways, and immunotherapy. The heterogeneity of tumors and the dynamic nature of epithelial plasticity in cancer cells make it likely that targeting only 1 EMT-related process will be unsuccessful or only transiently successful. We suggest that with greater understanding of epithelial plasticity regulation, such as with the EMT, a more systematic targeting of multiple EMT regulatory networks will be the best path forward to improve cancer outcomes.

scholarly journals GPCRomics: GPCR Expression in Cancer Cells and Tumors Identifies New, Potential Biomarkers and Therapeutic Targets

2018 ◽  
Vol 9 ◽  
Author(s):  
Paul A. Insel ◽  
Krishna Sriram ◽  
Shu Z. Wiley ◽  
Andrea Wilderman ◽  
Trishna Katakia ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Therapeutic Targets ◽  
Potential Biomarkers

scholarly journals Metabolic Alterations in Cancer and Their Potential as Therapeutic Targets

2017 ◽  
Vol 37 ◽  
pp. 825-832 ◽  
Author(s):  
Jamie D. Weyandt ◽  
Craig B. Thompson ◽  
Amato J. Giaccia ◽  
W. Kimryn Rathmell
Keyword(s):  
Therapeutic Targets ◽  
Metabolic Alterations

Cancer cell niche factors secreted from cancer-associated fibroblast by loss of H3K27me3

Gut ◽  
2019 ◽  
Vol 69 (2) ◽  
pp. 243-251 ◽  
Author(s):  
Masahiro Maeda ◽  
Hideyuki Takeshima ◽  
Naoko Iida ◽  
Naoko Hattori ◽  
Satoshi Yamashita ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Stem Cell ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stem Cell Niche ◽  
Therapeutic Targets ◽  
Prognostic Impact ◽  
Cell Growth And Migration ◽  
Cell Niche

ObjectiveCancer-associated fibroblasts (CAFs), a major component of cancer stroma, can confer aggressive properties to cancer cells by secreting multiple factors. Their phenotypes are stably maintained, but the mechanisms are not fully understood. We aimed to show the critical role of epigenetic changes in CAFs in maintaining their tumour-promoting capacity and to show the validity of the epigenomic approach in identifying therapeutic targets from CAFs to starve cancer cells.DesignTwelve pairs of primary gastric CAFs and their corresponding non-CAFs (NCAFs) were established from surgical specimens. Genome-wide DNA methylation and H3K27me3 analyses were conducted by BeadArray 450K and ChIP-on-Chip, respectively. Functions of potential a therapeutic target were analysed by inhibiting it, and prognostic impact was assessed in a database.ResultsCAFs had diverse and distinct DNA methylation and H3K27me3 patterns compared with NCAFs. Loss of H3K27me3, but not DNA methylation, in CAFs was enriched for genes involved in stem cell niche, cell growth, tissue development and stromal–epithelial interactions, such asWNT5A,GREM1,NOGandIGF2. Among these, we revealed that WNT5A, which had been considered to be derived from cancer cells, was highly expressed in cancer stromal fibroblasts, and was associated with poor prognosis. Inhibition of secreted WNT5A from CAFs suppressed cancer cell growth and migration.ConclusionsH3K27me3 plays a crucial role in defining tumour-promoting capacities of CAFs, and multiple stem cell niche factors were secreted from CAFs due to loss of H3K27me3. The validity of the epigenetic approach to uncover therapeutic targets for cancer-starving therapy was demonstrated.

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