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14-3-3eta inhibits LDHA by direct interaction in the setting of complex I dysfunction, highlighting the role of 14-3-3eta overexpression and inefficient oxidative phosphorylation in oncocytoma mitochondrial biogenesis.
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Results indicate that LDHA modulates autophagy by interacting with Beclin-1 in tamoxifen resistant breast cancer cells. Further data confirmed the association of LDHA in apoptosis resistance, increasing of EMT like phenomena and augmented pro-survival autophagy leading to the enhanced survivability of tamoxifen-resistant breast cancer.
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we demonstrate here that inhibition with siRNA against the glycolytic genes PFKFB3 or LDHA, respectively, prevents the proliferation of HUVECs and inhibits vessel formation in vitro as well as in vivo.
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LDHA inhibition fails to impact human melanoma cell proliferation, survival, or tumor growth. Reduced intracellular serine and aspartate following LDHA inhibition engage GCN2-ATF4 signaling to initiate an expansive pro-survival response.
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Our results indicate that ectopic FGFR1 expression reprograms the energy metabolism of prostate cancer cells, representing a hallmark change in prostate cancer progression. FGF signaling drives the Warburg effect through differential regulation of LDHA and LDHB, thereby promoting the progression of prostate cancer
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In patients treated with ipilimumab and nivolumab, baseline S100B and increasing S100B levels of >145% as well as baseline LDH were associated with impaired overall survival (OS) whereas increasing LDH of >25% was not (P = .64). S100B could serve as a strong baseline marker for OS in melanoma patients receiving anti-PD-1 therapy.
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Knockdown of LDHA by siRNA inhibits the migration and invasion via downregulation of glycolysis in ErbB2 over expressing breast cancer cell line
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the present study reports that the combination of tumour stroma percentage and tumour cell expression of cytoplasmic MCT-2 or nuclear LDH-5 is associated with poor prognosis.
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Serum LDH levels at baseline before nivolumab treatment were associated with the objective response and clinical outcome of nivolumab treatment
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LDHA promotes malignant behavior via activation of epithelial-to-mesenchymal transition in lung adenocarcinoma.
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Knockout of both LDH-A and LDH-B leads to suppression of glycolysis.
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LDHA and LDHB are dispensable for aerobic glycolysis in neuroblastoma cells while promoting their aggressiveness.
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Oligometastatic disease is not always correctly diagnosed, because all radiological modalities are limited by certain thresholds for detection of small metastases. We hypothesize that LDH is associated with survival, because this biomarker may reflect the total burden of malignant disease.
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Repression of LDHA induced by wt-p53 blocks tumor growth and invasion through downregulation of aerobic glycolysis in breast cancer.
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Data show that the 3'-untranslated region (3'-UTR) of LDHA mRNA was the direct target of microRNA-30d-5p (miR-30d-5p), which was low expressed in gallbladder cancer (GBC) tissues and associated with poor prognosis of GBC patients.
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e evaluated the link between mTOR kinase activity and the level of LDH expression / function. Furthermore, we elaborated the metabolic changes produced in cells by the mTOR-directed LDH-A up-regulation. Interestingly, we observed that in the non-neoplastic MCF-10A culture, mTOR-directed up-regulation of LDH-A was followed by a reprogramming of cell metabolism, which showed an increased dependence on glycolysis rather tha
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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.