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Tumor LDH-A expression, serum LDH status, and the slope of serum LDH status were closely associated with triple negative breast cancer brain metastasis and brain metastasis free survival. This study indicates that tumor LDH and serum LDH status are two predictors for triple negative breast cancer brain metastasis.
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Study revealed that LDHA expression was dysregulated in invasive pituitary adenoma (PA). In addition, LDHA was demonstrated to play an important role in invasion as well as PA growth.
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The study reveals that miR-33b plays a suppressive role in the regulation of osteosarcoma cell proliferation through direct targeting LDHA.
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hCINAP determines self-renewal of colorectal cancer stem cells by facilitating LDHA phosphorylation.
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the results of the present study demonstrated that miR199a3p can inhibit LDHA expression by downregulating Sp1, and provided mechanistic evidence supporting the existence of a novel miR199a3p/Sp1/LDHA axis and its critical contribution to aerobic glycolysis in testicular cancer cells.
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High LDHA expression is associated with Non-Small Cell Lung Cancer.
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This is the first study from this highly prevalent region of Head neck cancer showing that serum LDH could be regarded as a biomarker for malignant and premalignant conditions of the head and neck.
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High LDH expression is associated with small cell lung cancer.
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The PFK2 expression along with LDH-4 were observed to be increased ~2-fold (P < 0.001) in 0.5 mM ammonia treated brain slices.
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miR-199a-3p is a major metabolic regulator in tumor suppression and miR-199a-3p may downregulate metabolic genes (LDHA, PGK1, MCT1, TIGAR) through the transcription factor Sp1.
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The expression of LDH-5 and hypoxia-inducible factor (HIF) 1alpha in Non-Hodgkin's lymphoma, was examined.
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Results show that LDHA is highly expressed in triple negative breast cancer (TNBC) and correlated with a poor outcome. Its 3'UTR is targeted by miR-34a. Also, LDHA along with PDL1 seem to act as ceRNAs to promote the expression and function of each other through regulation of miR-34a in TNBC.
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LDHA siRNA can inhibit cell proliferation, induce apoptosis, reduce invasion and migration in renal cell carcinoma cells.
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JMJD2A regulated aerobic glycolysis by regulating LDHA expression. Therefore, the novel JMJD2A-LDHA signaling pathway could contribute to the Warburg effects in NPC progression.
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The present study proved that HIF1/2alpha could activate LDHA expression in human pancreatic cancer cells, and high expression of LDHA promoted the growth and migration of pancreatic cancer cells.
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Pretreatment LDH levels had noticeable prognostic value in advanced pancreatic ductal adenocarcinoma (PDAC) patients who received subsequent chemotherapy. Tackling elevated LDH levels before the initiation of chemotherapy might be a promising measure for improving overall survival of patients after treatment for their advanced PDAC.
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Authors demonstrated that knock down of LDHA with siRNA or inhibition of LDHA activity with a LDHA specific inhibitor (FX-11), could sensitize PC-3RR cells to radiotherapy with reduced epithelial-mesenchymal transition, hypoxia, DNA repair ability and autophagy, as well as increased DNA double strand breaks and apoptosis.
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Taken together, these results indicate that miR-142-3p could act as a tumor suppressor in HCC by targeting LDHA, suggesting new therapeutic targets for HCC treatment.
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Findings suggest that miR-34b-3 and miR-449a suppress the development of nasopharyngeal carcinoma (NPC) through regulation of glycolysis via targeting lactate dehydrogenase A.(LDHA) and may be potential therapeutic targets for the treatment of NPC.
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Results provide evidence that miR-200b acts as a tumor suppressor in glioma through the inhibition of LDHA both in vitro and in vivo.