Interplay Between Metabolism and Oncogenic Process: Role of
                        microRNAs

Arora, Aastha; Singh, Saurabh; Bhatt, Anant Narayan; Pandey, Sanjay; Sandhir, Rajat; Dwarakanath, Bilikere S.

doi:10.4137/tog.s29652

Cited by 35 publications

(22 citation statements)

References 220 publications

(224 reference statements)

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“…A number of cancer associated mutations affect metabolism and defects in mitochondria are seen in cancer that also link metabolism with cancer initiation and progression. Recent studies have shown that changes in cellular metabolism can alter the expression of specific microRNAs and promote epigenetic changes in tumor cells (Arora et al, 2015; Bishop and Ferguson, 2015; Chan et al, 2015). Although some of these interactions are mentioned above, in-depth discussions of all of the interactions that occur between cancer and metabolism are beyond the scope of this review and the reader is referred to a number of reviews on these subjects (Gatenby and Gillies, 2004; Vander Heiden et al, 2009; Cantor and Sabatini, 2012; Ward and Thompson, 2012; Semenza, 2013; Gaude and Frezza, 2014; Masson and Ratcliffe, 2014; Boroughs and DeBerardinis, 2015; Casey et al, 2015; Robey et al, 2015; Asati et al, 2016; Barron et al, 2016; Bost et al, 2016; Molon et al, 2016; Pavlova and Thompson, 2016; Pérez-Escuredo et al, 2016).…”

Section: Tumor Metabolismmentioning

confidence: 99%

Tumor Metabolism, the Ketogenic Diet and β-Hydroxybutyrate: Novel Approaches to Adjuvant Brain Tumor Therapy

Woolf

Syed

Scheck

2016

Front. Mol. Neurosci.

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Malignant brain tumors are devastating despite aggressive treatments such as surgical resection, chemotherapy and radiation therapy. The average life expectancy of patients with newly diagnosed glioblastoma is approximately ~18 months. It is clear that increased survival of brain tumor patients requires the design of new therapeutic modalities, especially those that enhance currently available treatments and/or limit tumor growth. One novel therapeutic arena is the metabolic dysregulation that results in an increased need for glucose in tumor cells. This phenomenon suggests that a reduction in tumor growth could be achieved by decreasing glucose availability, which can be accomplished through pharmacological means or through the use of a high-fat, low-carbohydrate ketogenic diet (KD). The KD, as the name implies, also provides increased blood ketones to support the energy needs of normal tissues. Preclinical work from a number of laboratories has shown that the KD does indeed reduce tumor growth in vivo. In addition, the KD has been shown to reduce angiogenesis, inflammation, peri-tumoral edema, migration and invasion. Furthermore, this diet can enhance the activity of radiation and chemotherapy in a mouse model of glioma, thus increasing survival. Additional studies in vitro have indicated that increasing ketones such as β-hydroxybutyrate (βHB) in the absence of glucose reduction can also inhibit cell growth and potentiate the effects of chemotherapy and radiation. Thus, while we are only beginning to understand the pluripotent mechanisms through which the KD affects tumor growth and response to conventional therapies, the emerging data provide strong support for the use of a KD in the treatment of malignant gliomas. This has led to a limited number of clinical trials investigating the use of a KD in patients with primary and recurrent glioma.

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Section: Tumor Metabolismmentioning

confidence: 99%

Tumor Metabolism, the Ketogenic Diet and β-Hydroxybutyrate: Novel Approaches to Adjuvant Brain Tumor Therapy

Woolf

Syed

Scheck

2016

Front. Mol. Neurosci.

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“…This metabolic shift contributes to excess glycolytic flux, lactate, low pH, activation of oncogenes and suppression of tumor suppressor genes. Glycolytic switch in cancer cells together with tumor secreted growth factors and TME drives angiogenesis in tumors by reprogramming EC metabolism and angiogenic signaling in EC [173,174]. miRNA which are angiogenic also participate in the regulation of EC metabolism.…”

Section: Discussion and Concluding Remarksmentioning

confidence: 99%

Anti-Angiogenic Effects of Phytochemicals on miRNA Regulating Breast Cancer Progression

et al. 2020

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Several phytochemicals have been identified for their role in modifying miRNA regulating tumor progression. miRNAs modulate the expression of several oncogenes and tumor suppressor genes including the genes that regulate tumor angiogenesis. Hypoxia inducible factor-1 alpha (HIF-1α) signaling is a central axis that activates oncogenic signaling and acts as a metabolic switch in endothelial cell (EC) driven tumor angiogenesis. Tumor angiogenesis driven by metabolic reprogramming of EC is crucial for tumor progression and metastasis in many different cancers, including breast cancers, and has been linked to aberrant miRNA expression profiles. In the current article, we identify different miRNAs that regulate tumor angiogenesis in the context of oncogenic signaling and metabolic reprogramming in ECs and review how selected phytochemicals could modulate miRNA levels to induce an anti-angiogenic action in breast cancer. Studies involving genistein, epigallocatechin gallate (EGCG) and resveratrol demonstrate the regulation of miRNA-21, miRNA-221/222 and miRNA-27, which are prognostic markers in triple negative breast cancers (TNBCs). Modulating the metabolic pathway is a novel strategy for controlling tumor angiogenesis and tumor growth. Cardamonin, curcumin and resveratrol exhibit their anti-angiogenic property by targeting the miRNAs that regulate EC metabolism. Here we suggest that using phytochemicals to target miRNAs, which in turn suppresses tumor angiogenesis, should have the potential to inhibit tumor growth, progression, invasion and metastasis and may be developed into an effective therapeutic strategy for the treatment of many different cancers where tumor angiogenesis plays a significant role in tumor growth and progression.

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“…MiRs are involved in the regulation of cell development, differentiation, proliferation, and apoptosis, and are closely related to the occurrence and development of many diseases [22]. MiR-21 is an oncogenic miR in human malignant tumors, and it is the only miR known to be highly expressed in almost all solid tumors [23, 24].…”

Section: Discussionmentioning

confidence: 99%

Role of microRNA-21 in radiosensitivity in non-small cell lung cancer cells by targeting PDCD4 gene

Jiang

Zhu

2017

Oncotarget

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This study aims to explore the effects of microRNA-21 (miR-21) on radiosensitivity in non-small cell lung cancer (NSCLC) by targeting programmed cell deanth 4 (PDCD4) and regulating PI3K/AKT/mTOR signaling pathway. Cancer tissues and adjacent normal tissues were collected from 97 NSCLC patients who received a standard radiotherapy regimen. TUNEL assay was applied to determine cell apoptosis in tissues. The qRT-PCR assay was used to detect the expressions of miR-21 expression and PDCD4 mRNA. The protein expressions of PDCD4 and PI3K/AKT/mTOR signaling pathway-related proteins were determined by Western blotting. Colony formation assay was used to observe the sensitivity to radiotherapy of NSCLC cells. Flow cytometry was adopted to testify cell apoptosis. Compared with adjacent normal tissues, miR-21 expression was significantly increased and the mRNA and protein expressions of PDCD4 were decreased in NSCLC tissues. Higher miR-21 expression was associated with attenuated radiation efficacy and shorter median survival time. PDCD4 was the target gene of miR-21. The miR-21 mimics and siRNA-PDCD4 decreased the sensitivity to radiotherapy and cell apoptosis of A549 and H1299 cells and activated PI3K/AKT/mTOR pathway. The sensitivity of A549 and H1299 cells was strengthened in the miR-21 inhibitors group and the PI3K/AKT/mTOR inhibitors group. The siRNA-PDCD4 could reverse the effects of miR-21 inhibitors on sensitivity to radiotherapy and cell apoptosis of NSCLC cells. Our findings provide strong evidence that miR-21 could inhibit PDCD4 expression and activate PI3K/AKT/mTOR signaling pathway, thereby affecting the radiation sensitivity of NSCLC cells.

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Interplay Between Metabolism and Oncogenic Process: Role of microRNAs

Cited by 35 publications

References 220 publications

Tumor Metabolism, the Ketogenic Diet and β-Hydroxybutyrate: Novel Approaches to Adjuvant Brain Tumor Therapy

Tumor Metabolism, the Ketogenic Diet and β-Hydroxybutyrate: Novel Approaches to Adjuvant Brain Tumor Therapy

Anti-Angiogenic Effects of Phytochemicals on miRNA Regulating Breast Cancer Progression

Role of microRNA-21 in radiosensitivity in non-small cell lung cancer cells by targeting PDCD4 gene

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