Silencing PFKP inhibits starvation-induced autophagy, glycolysis, and epithelial mesenchymal transition in oral squamous cell carcinoma

Chen, Guanhui; Liu, Haichao; Zhang, Yadong; Liang, Jianfeng; Zhu, Yue; Zhang, Ming; Yu, Dongsheng; Wang, Cheng; Hou, Jinsong

doi:10.1016/j.yexcr.2018.06.007

Cited by 64 publications

(47 citation statements)

References 38 publications

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“… 48 Remarkably, a recent study reported that the knockdown of PFKP in oral squamous cell carcinoma dramatically inhibited the expression of LC3-II and Atg5, as well as decreased starvation-mediated glycolysis and autophagy, indicating that PFKP is necessary for starvation-mediated autophagy and glycolysis. 49 Differently, in this study, we found that transfecting VSMCs with Sal-miR-58 significantly attenuated the level of PFKP protein, and downregulation of PFKP induced VSMC autophagy. This discrepancy in the effect of PFKP on autophagy between the studies might be due to differences in the context of autophagy between cancer cells and VSMCs used in the experiments.…”

Section: Discussionmentioning

confidence: 49%

Salvia miltiorrhiza-Derived Sal-miR-58 Induces Autophagy and Attenuates Inflammation in Vascular Smooth Muscle Cells

Qin

Zheng

Yang

et al. 2020

Molecular Therapy - Nucleic Acids

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Section: Discussionmentioning

confidence: 49%

Salvia miltiorrhiza-Derived Sal-miR-58 Induces Autophagy and Attenuates Inflammation in Vascular Smooth Muscle Cells

Qin

Zheng

Yang

et al. 2020

Molecular Therapy - Nucleic Acids

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“…In addition, previous studies have shown that high FBP1 expression inhibits tumor growth by hindering epithelial-mesenchymal transition (EMT) 33 , and degradation of FBP1 promotes tumor progression by altering the Warburg effect in hepatocellular carcinoma cells 34 . PFKP (phosphofructokinase, platelet) is an isoform of phosphofructokinase, which plays a vital role in glycolysis regulation and metabolic reprogramming in many cancers including ccRCC 35 , 36 . LGALS1 (galectin 1) is a β-galactoside-binding protein that recognizes glycoconjugates and regulates cell proliferation, differentiation and apoptosis in cancer 37 .…”

Section: Discussionmentioning

confidence: 99%

Identification of a Glucose Metabolism-related Signature for prediction of Clinical Prognosis in Clear Cell Renal Cell Carcinoma

Wang¹,

Zhang²,

Yu³

et al. 2020

J. Cancer

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Background: Clear cell renal cell carcinoma (ccRCC) is one of the most prevalent and invasive histological subtypes among all renal cell carcinomas (RCC). Cancer cell metabolism, particularly glucose metabolism, has been reported as a hallmark of cancer. However, the characteristics of glucose metabolism-related gene sets in ccRCC have not been systematically profiled. Methods: In this study, we downloaded a gene expression profile and glucose metabolism-related gene set from TCGA (The Cancer Genome Altas) and MSigDB, respectively, to analyze the characteristics of glucose metabolism-related gene sets in ccRCC. We used a multivariable Cox regression analysis to develop a risk signature, which divided patients into low- and high- risk groups. In addition, a nomogram that combined the risk signature and clinical characteristics was created for predicting the 3- and 5-year overall survival (OS) of ccRCC. The accuracy of the nomogram prediction was evaluated using the area under the receiver operating characteristic curve (AUC) and a calibration plot. Results: A total of 231 glucose metabolism-related genes were found, and 68 differentially expressed genes (DEGs) were identified. After screening by univariate regression analysis, LASSO regression analysis and multivariable Cox regression analysis, six glucose metabolism-related DEGs ( FBP1, GYG2, KAT2A, LGALS1, PFKP, and RGN ) were selected to develop a risk signature. There were significant differences in the clinical features (Fuhrman nuclear grade and TNM stage) between the high- and low-risk groups. The multivariable Cox regression indicated that the risk score was independent of the prognostic factors (training set: HR=3.393, 95% CI [2.025, 5.685], p<0.001; validation set: HR=1.933, 95% CI [1.130, 3.308], p=0.016). The AUCs of the nomograms for the 3-year OS in the training and validation sets were 0.808 and 0.819, respectively, and 0.777 and 0.796, respectively, for the 5- year OS. Conclusion: We demonstrated a novel glucose metabolism-related risk signature for predicting the prognosis of ccRCC. However, additional in vitro and in vivo research is required to validate our findings.

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“…Aerobic glycolysis, i.e., the Warburg effect, constitutes one of its important features during the development of OSCC (3)(4)(5). Cancer cells enhance glucose uptake and lactate production through aerobic glycolysis to meet energy metabolism and biosynthesis needs.…”

Section: Introductionmentioning

confidence: 99%

LDHA Promotes Oral Squamous Cell Carcinoma Progression Through Facilitating Glycolysis and Epithelial–Mesenchymal Transition

Cai

Zhang

et al. 2019

Front. Oncol.

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Aerobic glycolysis is the main pathway for energy metabolism in cancer cells. It provides energy and biosynthetic substances for tumor progression and metastasis by increasing lactate production. Lactate dehydrogenase A (LDHA) promotes glycolysis process by catalyzing the conversion of pyruvate to lactate. Despite LDHA exhibiting carcinogenesis in various cancers, its role in oral squamous cell carcinoma (OSCC) remains unclear. This study demonstrated that LDHA was over-expressed in both OSCC tissues and cell lines, and was significantly associated with lower overall survival rates in patients with OSCC. Using weighted gene correlation network analysis and gene set enrichment analysis for the gene expression data of patients with OSCC (obtained from The Cancer Genome Atlas database), a close association was identified between epithelial-mesenchymal transition (EMT) and LDHA in promoting OSCC progression. The knockdown of LDHA suppressed EMT, cell proliferation, and migration and invasion of OSCC cells in vitro. Moreover, the silencing of LDHA inhibited tumor growth in vivo. Oxamate, as a competitive LDHA inhibitor, was also suppressed diverse malignant biocharacteristics of OSCC cells. Our findings reveal that LDHA acts as an oncogene to promote malignant progression of OSCC by facilitating glycolysis and EMT, and LDHA may be a potential anticancer therapeutic target.

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Silencing PFKP inhibits starvation-induced autophagy, glycolysis, and epithelial mesenchymal transition in oral squamous cell carcinoma

Cited by 64 publications

References 38 publications

Salvia miltiorrhiza-Derived Sal-miR-58 Induces Autophagy and Attenuates Inflammation in Vascular Smooth Muscle Cells

Salvia miltiorrhiza-Derived Sal-miR-58 Induces Autophagy and Attenuates Inflammation in Vascular Smooth Muscle Cells

Identification of a Glucose Metabolism-related Signature for prediction of Clinical Prognosis in Clear Cell Renal Cell Carcinoma

LDHA Promotes Oral Squamous Cell Carcinoma Progression Through Facilitating Glycolysis and Epithelial–Mesenchymal Transition

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