MiR-200c inhibited the proliferation of oral squamous cell carcinoma cells by targeting Akt pathway and its downstream Glut1

Yan, Yixuan; Yan, Fengzhi; Huang, Qun

doi:10.1016/j.archoralbio.2018.06.003

Cited by 19 publications

(12 citation statements)

References 17 publications

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“…Several rate-limiting enzymes such as GLUT1, HK2, PFK1 and G6PD play crucial roles during these glucose metabolism processes (27). Previous studies have shown that these enzymes are regulated directly or indirectly by miRNAs (28)(29)(30)(31)(32). The present results indicated that the expression levels of these enzymes were decrease by miR-218 in NSCLC cell lines.…”

Section: Discussionsupporting

confidence: 58%

miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway

et al. 2020

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High glucose metabolism is recognized as one of the hallmarks of cancer and increased expression levels of several key factors involved in glucose metabolism have been reported in non-small cell lung cancer (NSCLC). Previous studies showed that microRNA (miR)-218 is reduced in NSCLC, but its function in glucose metabolism in NSCLC is not fully understood. The present study aimed to investigate the effect of miR-218 on glucose metabolism in NSCLC cell lines and the underlying molecular mechanism. The present results suggested that miR-218 reduced glucose consumption, the mechanism of glycolysis and activity in the pentose phosphate pathway. In addition, glucose transporter 1 (GLUT1) was identified to be a direct target of miR-218, while overexpression of GLUT1 did not abolish the effect of miR-218 on glucose metabolism. The present results indicated that phosphorylation of NF-κB p65 was significantly decreased by miR-218 in NSCLC cells and that activation of NF-κB led to the inhibition of miR-218 regulation of glucose metabolism. In conclusion, the present results suggested that miR-218 downregulated glucose metabolism in NSCLC not only by directly targeting GLUT1, but also via the NF-κB signaling pathway.

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Section: Discussionsupporting

confidence: 58%

miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway

et al. 2020

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“…Extensive observations have reported that the upregulation of Akt contributes to the occurrence and development of multiple cancers, indicating that Akt is considered as a therapeutic target for tumors [36][37][38]. Therefore, Akt has been shown to function as an oncogene in cancer progression, including OSCC [39,40]. Recent studies aimed to explore the Akt toward the molecular targeted treatment using small-molecule inhibitors in human tumors.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol acts via melanoma-associated antigen A12 (MAGEA12)/protein kinase B (Akt) signaling to inhibit the proliferation of oral squamous cell carcinoma cells

Shang

Jiang

et al. 2021

Bioengineered

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“…Glucose transporters, as mentioned above, are associated with glucose uptake in cells and their upregulation is a hallmark of the Warburg phenotype in cancer cells. Many experimental studies suggest an association between miRNA deregulation and GLUT1 activity including upregulation of miR-150 [ 59 ], miR-522-3p [ 60 ] and miR-10a [ 61 ], whereas expression rates of miR-340 [ 62 ], miR-218 [ 63 ] and miR-200c [ 64 ] are reduced.…”

Section: Molecular View Into the Warburg Effectmentioning

confidence: 99%

Flavonoids against the Warburg phenotype—concepts of predictive, preventive and personalised medicine to cut the Gordian knot of cancer cell metabolism

et al. 2020

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The Warburg effect is characterised by increased glucose uptake and lactate secretion in cancer cells resulting from metabolic transformation in tumour tissue. The corresponding molecular pathways switch from oxidative phosphorylation to aerobic glycolysis, due to changes in glucose degradation mechanisms known as the 'Warburg reprogramming' of cancer cells. Key glycolytic enzymes, glucose transporters and transcription factors involved in the Warburg transformation are frequently dysregulated during carcinogenesis considered as promising diagnostic and prognostic markers as well as treatment targets. Flavonoids are molecules with pleiotropic activities. The metabolism-regulating anticancer effects of flavonoids are broadly demonstrated in preclinical studies. Flavonoids modulate key pathways involved in the Warburg phenotype including but not limited to PKM2, HK2, GLUT1 and HIF-1. The corresponding molecular mechanisms and clinical relevance of 'anti-Warburg' effects of flavonoids are discussed in this review article. The most prominent examples are provided for the potential application of targeted 'anti-Warburg' measures in cancer management. Individualised profiling and patient stratification are presented as powerful tools for implementing targeted 'anti-Warburg' measures in the context of predictive, preventive and personalised medicine.

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MiR-200c inhibited the proliferation of oral squamous cell carcinoma cells by targeting Akt pathway and its downstream Glut1

Cited by 19 publications

References 17 publications

miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway

miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway

Resveratrol acts via melanoma-associated antigen A12 (MAGEA12)/protein kinase B (Akt) signaling to inhibit the proliferation of oral squamous cell carcinoma cells

Flavonoids against the Warburg phenotype—concepts of predictive, preventive and personalised medicine to cut the Gordian knot of cancer cell metabolism

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