&lt;p&gt;Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma&lt;/p&gt;

Han, Wei; Shi, Jia; Cao, Jiachao; Dong, Bo; Guan, Wei

doi:10.2147/ott.s260376

Cited by 28 publications

(16 citation statements)

References 213 publications

(317 reference statements)

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“…Glioma is one of the most malignant and aggressive type of primary brain tumor (H. Chen et al, 2019). The prognosis of glioma is poor, despite the progress in therapeutic strategies, including surgery resection, chemotherapy, and radiotherapy (Han et al, 2020). Although the mechanism in the tumorigenesis of glioma remains unclear, the role of circRNAs in cancer development and progression has raised many concerns currently.…”

Section: Discussionmentioning

confidence: 99%

“…The current standard management of GBM is a combined treatment based on surgery and including radiotherapy and chemotherapy. However, due to the infiltrative growth, resistance to therapies, and intra‐ and intertumoral genetic heterogeneity, GBM has a high recurrence rate (W. Han et al, 2020). The results of treatment are still not satisfactory.…”

Section: Introductionmentioning

confidence: 99%

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Circular RNA circHECTD1 facilitates glioma progression by regulating the miR‐296‐3p/SLC10A7 axis

Liu

et al. 2021

Journal Cellular Physiology

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Glioma is the most common type of primary brain tumor. Treatment options for recurrent gliomas include surgery, chemotherapy, and radiation therapy, but the clinical outcome is usually limited. In recent years, circular RNAs have been found to play a vital role in several human cancers. Gene Expression Omnibus database was utilized to verify the differentially expressed circRNAs. Then we detected that the expression of circular RNA circHECTD1 was significantly increased. The expression and function of circHECDT1 has not yet been reported in glioma. Then we confirmed that the level of circHECTD1 was significantly increased both in glioma tissues and cell lines, which is negatively correlated with the overall survival of patients. Knockdown of circHECTD1 inhibited proliferation and invasion in vitro, and also reduced the growth of tumor and prolonged the prognosis in vivo. Knockdown of circHECTD1 significantly elevated the miR‐296‐3p expression in LN229 and T98G cells. Luciferase reports and RNA immunoprecipitation data indicated that miR‐296‐3p was a direct target of circHECTD1 and that the miR‐296‐3p expression negatively regulated SLC10A7. Rescue experiments showed that the overexpression of SLC10A7 could impede the effects of circHECTD1 silencing on the proliferation and invasion of glioma cells. In this study, we identified that circHECTD1 regulates SLC10A7 by interacting with miR‐296‐3p in glioma cells. In conclusion, this study investigated a novel biomarker panel consisting of the circHECTD1/miR‐296‐3p/SLC10A7 axis, which is critical for glioma tumorigenesis and invasiveness and may represent a novel therapeutic target for intervening in glioma progression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Circular RNA circHECTD1 facilitates glioma progression by regulating the miR‐296‐3p/SLC10A7 axis

Liu

et al. 2021

Journal Cellular Physiology

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“…These data suggested that UBE2D3 exerted functions in glioma via SHP-2. Activated glycolysis is reported to be associated with the progression of glioma (24). The blockade of glucose transporters and glycolytic enzymes exhibited promising anticancer effects in preclinical models (15).…”

Section: Discussionmentioning

confidence: 99%

UBE2D3 Activates SHP-2 Ubiquitination to Promote Glycolysis and Proliferation of Glioma via Regulating STAT3 Signaling Pathway

Pan¹,

Bao²,

Zhang³

et al. 2021

Front. Oncol.

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Glioma is a primary brain cancer with high malignancy and morbidity. Current management for glioma cannot reach optimal remission. Therefore, it is necessary to find novel targets for glioma treatment. Ubiquitin-conjugating enzyme E2 D3 (UBE2D3) is involved in the pathogenesis of various kinds of cancer. However, its role in glioma remains unclear. Our study aims to explore the function and underlying mechanism of UBE2D3 in the development of glioma. By analysis with The Cancer Genome Atlas-Glioblastoma multiforme (TCGA-GBM) dataset, we found that UBE2D3 was highly expressed in glioma and it is positive correlation with glycolysis, apoptosis, and STAT3 pathway. Then, we explore the effects of UBE2D3 knockdown in the biological functions of glioma cell lines. Cell proliferation and apoptosis were estimated by cell counting kit-8 assay and flow cytometry. Extracellular acidification rate and oxygen consumption rate were estimated to determine the level of cell glycolysis. Xenograft experiments were performed to identify in vivo function of UBE2D3. The results showed that the inhibition of UBE2D3 could suppress the proliferation, glycolysis, and STAT3 phosphorylation of GBM both in vitro and in vivo. UBE2D3 could interact with SHP-2 and promoted its ubiquitination, which elevated the activation of STAT3 pathway. Overexpressed SHP-2 could reverse the effect of UBE2D3 and they shared contrary expression patterns in glioma and normal brain tissues. In summary, our study revealed that UBE2D3 could promote the ubiquitination of SHP-2, which activated STAT3 pathway and promoted glioma proliferation as well as glycolysis. UBE2D3 could be a potential target for glioma treatment.

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“…One of the main early cellular events evoked upon exposure to hypoxia is the activation of hypoxia-inducible factor 1 (HIF-1) [ 5 ], an oxygen-regulated transcription factor that mediates the adaptation of cells to decreased oxygen supply. On the other hand, accumulating studies have demonstrated that accelerated aerobic glycolysis, also known as the Warburg effect, participates in the clinical aggressiveness of tumors including gliomas [ 6 ]. In contrast to normal cells, malignant cells use pyruvate for energy production instead of fluxing it into acetyl-CoA in the tricarboxylic acid (TCA) cycle, even under normoxic conditions.…”

Section: Introductionmentioning

confidence: 99%

“…The rate of glucose metabolism through aerobic glycolysis is higher, so the production of lactate from glucose occurs much faster than the complete oxidation of glucose in the TCA cycle at the expense of inefficient ATP production [ 7 ]. As a result, cancer cells overexpress glucose transporters to compensate for their high energy demand with their abnormally high rate of glucose uptake [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia and glucose metabolism assessed by FMISO and FDG PET for predicting IDH1 mutation and 1p/19q codeletion status in newly diagnosed malignant gliomas

et al. 2021

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Background Tumor hypoxia and glycolysis have been recognized as determinant factors characterizing tumor aggressiveness in malignant gliomas. To clarify in vivo hypoxia and glucose metabolism in relation to isocitrate dehydrogenase (IDH) mutation and chromosome 1p and 19q (1p/19q) codeletion status, we retrospectively analyzed hypoxia as assessed by positron emission tomography (PET) with [18F]-fluoromisonidazole (FMISO) and glucose metabolism as assessed by PET with [18F]-fluoro-2-deoxy-d-glucose (FDG) in newly diagnosed malignant gliomas. Methods In total, 87 patients with newly diagnosed supratentorial malignant (WHO grade III and IV) gliomas were enrolled in this study. They underwent PET studies with FMISO and FDG before surgery. The molecular features and histopathological diagnoses based on the 2016 WHO classification were determined using surgical specimens. Maximal tumor-to-normal ratio (TNR) was calculated for FDG PET, and maximal tumor-to-blood SUV ratio (TBR) was calculated for FMISO PET. The PET uptake values in relation to IDH mutation and 1p/19q codeletion status were statistically analyzed. Results In all tumors and malignant astrocytomas, the median FMISO TBR in IDH-wildtype tumors was significantly higher than that in IDH-mutant tumors (P < 0.001 and P < 0.01, respectively). In receiver operating characteristic (ROC) analysis, the area under the curve showed that the sensitivity for the discrimination was moderate (0.7–0.8) and the specificity was low (0.65–0.68). In the same population, the median FDG TNR in IDH-wildtype tumors tended to be higher than that in IDH-mutant tumors, but the difference was not statistically significant. In WHO grade III anaplastic astrocytomas, there were no significant differences in median FMISO TBR or FDG TNR between IDH-mutant and IDH-wildtype tumors. In IDH-mutant WHO grade III anaplastic gliomas, there were no significant differences in median FMISO TBR or FDG TNR between anaplastic astrocytomas and anaplastic oligodendrogliomas. Conclusions Tumor hypoxia as assessed by FMISO PET was informative for prediction of the IDH mutation status in newly diagnosed malignant gliomas. However, the accuracy of the discrimination was not satisfactory for clinical application. On the other hand, glucose metabolism as assessed by FDG PET could not differentiate the IDH-mutant status. Moreover, PET studies using FMISO and FDG could not predict IDH mutation and 1p/19q codeletion status in WHO grade III tumors.

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<p>Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma</p>

Cited by 28 publications

References 213 publications

Circular RNA circHECTD1 facilitates glioma progression by regulating the miR‐296‐3p/SLC10A7 axis

Circular RNA circHECTD1 facilitates glioma progression by regulating the miR‐296‐3p/SLC10A7 axis

UBE2D3 Activates SHP-2 Ubiquitination to Promote Glycolysis and Proliferation of Glioma via Regulating STAT3 Signaling Pathway

Hypoxia and glucose metabolism assessed by FMISO and FDG PET for predicting IDH1 mutation and 1p/19q codeletion status in newly diagnosed malignant gliomas

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