MiR-34a contributes to diabetes-related cochlear hair cell apoptosis via SIRT1/HIF-1α signaling

Lin, Ying; Shen, Jinjin; Li, Danfeng; Ming, Jie; Li, Xiangyang; Zhang, Nana; Lai, Jingbo; Shi, Min; Ji, Qiuhe; Xing, Ying

doi:10.1016/j.ygcen.2017.02.017

Cited by 37 publications

(24 citation statements)

References 31 publications

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“…HIF-1α directly repressed the MIR34A gene in p53-defective CRC cells, whereas expression of MIR34A was induced in p53-proficient CRC cells exposed to hypoxia. Downregulation of MIR34A was required for hypoxia-induced epithelial-mesenchymal transition, invasion and migration, and activation of signal transducer and activator of transcription in CRC cells [25,26]. Our results were similar.…”

Section: Discussionsupporting

confidence: 75%

Increased Lactate in Gastric Cancer Tumor-Infiltrating Lymphocytes Is Related to Impaired T Cell Function Due to miR-34a Deregulated Lactate Dehydrogenase A

Wang

Senyan

et al. 2018

Cell Physiol Biochem

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Background/Aims: Lactate is one of the products of glycolysis and is a hallmark of the Warburg effect. Glycolysis is found in tumor as well as immune cells. However, the effects of lactate on the function of tumor-infiltrating T cells (TILs) are rarely reported. Methods: In the present study, we investigated lactate and other glycolysis-related metabolites within TILs of human gastric cancer (GC). Lactate concentration was determined by liquid chromatography–mass spectrometry. The functional effects and clinical relevance of excessive lactate on T cells were investigated in clinical samples, and the mechanism of increased lactate was explored. Results: Lactate was significantly increased in GC TILs and related to decreased T helper (Th)1 cells and cytotoxic T lymphocytes (CTLs). Increased lactate within GC TILs was positively correlated with increased lactate dehydrogenase A (LDH)A. Expression of LDHA in GC TILs was also negatively correlated with percentages of Th1 cells and CTLs. Decreased miR-34a expression in GC TILs was responsible for increased expression of LDHA. A hypoxic tumor environment was responsible for decreased miR-34a and lactate-induced impaired immune function. Conclusion: We found that hypoxia decreases miR-34a expression and lose miR-34a regulation on LDHA, thus increasing lactate level within GC TILs and impairing immune function in GC.

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Section: Discussionsupporting

confidence: 75%

Increased Lactate in Gastric Cancer Tumor-Infiltrating Lymphocytes Is Related to Impaired T Cell Function Due to miR-34a Deregulated Lactate Dehydrogenase A

Wang

Senyan

et al. 2018

Cell Physiol Biochem

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“…An increasing number of studies have indicated that the pathogenic changes in various tissues are associated with miRs dysregulated expression via various cell signaling pathways [12][13][14]. The role of miR-34a in DM-related complications has been well documented, the targets of miR-34a, including SIRT1/HIF-1α, NOTCH andPERK/p53, have been defined [15][16][17]. Intriguingly, miR-34a expression is upregulated in HG-exposed mouse microvascular endothelial cells [18].…”

Section: Resultsmentioning

confidence: 99%

Intravenous Injection of miR-34a Inhibitor Alleviates Diabetes Mellitus-Induced Vascular Endothelial Dysfunction by Targeting NOTCH1

Zhao

Wang

et al. 2018

Exp Clin Endocrinol Diabetes

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“…miR-34a reportedly acts as a tumor suppressor in many cancers, including pancreatic cancer, prostate cancer, glioblastoma, colon cancer, and breast cancer ( 14 – 17 ). In pancreatic cancer, miR-34a inhibits stem cell self-renewal by downregulating Bcl-2 and Notch ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑34a inhibits liver cancer cell growth by reprogramming glucose metabolism

2018

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MicroRNAs (miRs) have been proposed as minimally invasive prognostic markers for various types of cancer, including liver cancer, which is one of the most common cancers worldwide. In the present study, the expression of miR-34a in human liver cancer tissues and cell lines was evaluated and the effects of miR-34a on cell proliferation, invasion and glycolysis in hepatocellular carcinoma (HCC) cells were determined. The results indicated that miR-34a was downregulated in human liver cancer tissues. Overexpression of miR-34a significantly inhibited liver cancer cell proliferation and clone formation. In terms of the underlying mechanism, miR-34a was indicated to negatively regulate the expression of lactate dehydrogenase A (LDHA), which consequently inhibited LDHA-dependent glucose uptake in the cancer cells, as well as cell proliferation and invasion. Collectively, these data suggest that miR-34a functions as a negative regulator of glucose metabolism and may serve as a novel marker for liver cancer prognosis.

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MiR-34a contributes to diabetes-related cochlear hair cell apoptosis via SIRT1/HIF-1α signaling

Cited by 37 publications

References 31 publications

Increased Lactate in Gastric Cancer Tumor-Infiltrating Lymphocytes Is Related to Impaired T Cell Function Due to miR-34a Deregulated Lactate Dehydrogenase A

Increased Lactate in Gastric Cancer Tumor-Infiltrating Lymphocytes Is Related to Impaired T Cell Function Due to miR-34a Deregulated Lactate Dehydrogenase A

Intravenous Injection of miR-34a Inhibitor Alleviates Diabetes Mellitus-Induced Vascular Endothelial Dysfunction by Targeting NOTCH1

MicroRNA‑34a inhibits liver cancer cell growth by reprogramming glucose metabolism

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