High expression of Aldolase A predicts poor survival in patients with clear-cell renal cell carcinoma

Na, Ning; Li, Heng; Xu, Chenyu; Miao, Benchun; Hong, Lei; Huang, Zhengyu; Qiu, Jian

doi:10.2147/tcrm.s123199

Cited by 17 publications

(16 citation statements)

References 27 publications

(42 reference statements)

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“…Aside from this, Na et al conducted multivariate analysis that revealed ALDOA as an independent and significant prognostic factor in clear cell renal cell carcinoma [18,19]. Herein we found that ALDOA was of much higher expression level in tumor tissues and cells than in normal tissues and cells.…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 50%

miR-122-5p Inhibits the Proliferation, Invasion and Growth of Bile Duct Carcinoma Cells by Targeting ALDOA

Liu

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Bile duct cancer, although not among the most common tumors, still accounts for more and more worldwide deaths each year. By attempting to verify an overexpression of ALDOA in cholangiocarcinoma tissues and cells and explore the underlying molecular mechanism regulated by miR-122-5p, this study was designed to provide a potential molecular target in bile duct cancer treatment. Methods: Western blot and immunohistochemistry were performed to detect the ALDOA protein level in duct carcinoma tissues. The transfection efficiency was confirmed by western blot and/or RT-qPCR assay. The proliferation of bile duct carcinoma cells was determined by MTT and colony formation assay. The invasion ability of bile duct carcinoma cells was evaluated with Transwell invasion assay. Flow cytometry detected cell apoptosis of bile duct carcinoma cells. The miRNAs which modulate ALDOA were filtrated from bioinformatics software and clinical specimens. The target relationship was confirmed by dual luciferase reporter assay. Furthermore, a xenograft model was completed to verify the impact of miRNA on inhibition growth of bile duct carcinoma cells. Results: ALDOA was found up-regulated in bile duct carcinoma tissues and cells. Knockdown of ALDOA promoted the apoptosis of cells and inhibited the proliferation and invasion of bile duct carcinoma cells. Bioinformatics and clinical specimens indicated the negative correlation and targeted regulation between miR-122-5p and ALDOA. By down-regulating ALDOA, overexpression of miR-122-5p appeared to promote cell apoptosis and significantly inhibit cell proliferation, invasion in vitro and suppress the tumor growth in vivo. Conclusion: miR-122-5p inhibited proliferation and invasion of bile duct carcinoma cells and promoted cell apoptosis by targeting ALDOA expression.

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Section: Cellular Physiology and Biochemistrysupporting

confidence: 50%

miR-122-5p Inhibits the Proliferation, Invasion and Growth of Bile Duct Carcinoma Cells by Targeting ALDOA

Liu

Zhang

et al. 2018

Cell Physiol Biochem

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“…This again indicates a critical metabolic change, as previously observed in chRCC (27) and in gastric cancer (35). Conversely, an over-expression of gluconeogenic genes and proteins is frequently found in other tumor species, such as the over-expression of ALDOB in ccRCC (36) and colon cancer (37)(38)(39), which was also associated with tumor progression and poor prognosis.…”

Section: Discussionsupporting

confidence: 73%

Papillary renal cell carcinomas rewire glutathione metabolism and are deficient in anabolic glucose synthesis

Alahmad

Paffrath

Clima

et al. 2019

Preprint

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Papillary renal cell carcinoma (pRCC) is a malignant kidney cancer with a prevalence of 7-20% of all renal tumors. Proteome and metabolome profiles of 19 pRCC and patient-matched healthy kidney controls were used to elucidate the regulation of metabolic pathways and the underlying molecular mechanisms. Glutathione (GSH), a main reactive oxygen species (ROS) scavenger, was highly increased and can be regarded as a new hallmark in this malignancy. Isotope tracing of pRCC derived cell lines revealed an increased de novo synthesis rate of GSH, based on glutamine consumption. Furthermore, rewiring of the main pathways involved in ATP and glucose synthesis was observed at the protein level. In contrast, transcripts encoding for the respiratory chain were not regulated, which prompts for non-genetic profiling. The molecular characteristics of pRCC are increased GSH synthesis to cope with ROS stress, deficient anabolic glucose synthesis, and compromised oxidative phosphorylation, which could potentially be exploited in innovative anti-cancer strategies.

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“…Also the up-regulation of ALDOA has been reported in many cancer types, such as oral squamous cell carcinoma [40], hepatocellular carcinoma [41], and in RCC [42] and of ALDOA in ccRCC [43], osteosarcoma [44], and lung cancer [45]. Specifically, an increase in ALDOA was shown for all RCC types and was associated with metastasis, histological differentiation, and poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Papillary Renal Cell Carcinomas Rewire Glutathione Metabolism and Are Deficient in Both Anabolic Glucose Synthesis and Oxidative Phosphorylation

Ahmad

Paffrath

Clima

et al. 2019

Cancers

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Papillary renal cell carcinoma (pRCC) is a malignant kidney cancer with a prevalence of 7–20% of all renal tumors. Proteome and metabolome profiles of 19 pRCC and patient-matched healthy kidney controls were used to elucidate the regulation of metabolic pathways and the underlying molecular mechanisms. Glutathione (GSH), a main reactive oxygen species (ROS) scavenger, was highly increased and can be regarded as a new hallmark in this malignancy. Isotope tracing of pRCC derived cell lines revealed an increased de novo synthesis rate of GSH, based on glutamine consumption. Furthermore, profound downregulation of gluconeogenesis and oxidative phosphorylation was observed at the protein level. In contrast, analysis of the The Cancer Genome Atlas (TCGA) papillary RCC cohort revealed no significant change in transcripts encoding oxidative phosphorylation compared to normal kidney tissue, highlighting the importance of proteomic profiling. The molecular characteristics of pRCC are increased GSH synthesis to cope with ROS stress, deficient anabolic glucose synthesis, and compromised oxidative phosphorylation, which could potentially be exploited in innovative anti-cancer strategies.

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High expression of Aldolase A predicts poor survival in patients with clear-cell renal cell carcinoma

Cited by 17 publications

References 27 publications

miR-122-5p Inhibits the Proliferation, Invasion and Growth of Bile Duct Carcinoma Cells by Targeting ALDOA

miR-122-5p Inhibits the Proliferation, Invasion and Growth of Bile Duct Carcinoma Cells by Targeting ALDOA

Papillary renal cell carcinomas rewire glutathione metabolism and are deficient in anabolic glucose synthesis

Papillary Renal Cell Carcinomas Rewire Glutathione Metabolism and Are Deficient in Both Anabolic Glucose Synthesis and Oxidative Phosphorylation

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