ALDOA functions as an oncogene in the highly metastatic pancreatic cancer

Ji, Shunrong; Zhang, Bo; Liu, Jiang; Qin, Yi; Liang, Chen; Shi, Si; Jin, Kaizhou; Liang, Dingkong; Xu, Wenyan; Xu, Huaxiang; Wang, Wenquan; Wu, Chifei; Liu, Liang; Liu, Chen; Xu, Jin; Ni, Quanxing

doi:10.1016/j.canlet.2016.01.054

Cited by 121 publications

(115 citation statements)

References 35 publications

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“…ALDOA is a ubiquitous glycolytic enzyme that drives the glycolytic metabolic pathway in mammalian cells. Aberrant expression of ALDOA was found in various cancers,15,17,18 suggesting enhanced glycolysis in these cancer cells. Abnormal expression of ALDOA was also observed in renal carcinoma by a recent proteotranscriptomic study, which revealed that ALDOA were decreased at early stages relative to normal tissue but increased at later stages 13.…”

Section: Discussionmentioning

confidence: 98%

“…In regard to biological functions, ALDOA has been identified as an oncogene in cancers such as, lung cancer,15,16 pancreatic ductal adenocarcinoma,17 and hepatocellular carcinomas 18. ALDOA was involved in the regulation of cell viability, proliferation ability, and metastasis capacity of many cancer cells; it also participated in activating signal pathways associated with tumorigenesis 25.…”

Section: Discussionmentioning

confidence: 99%

“…Aldolase A (ALDOA) is a key enzyme in glycolysis responsible for catalyzing the reversible conversion of fructose-1,6-bisphosphate to glyceraldehyde-3-phosphate and dihydroxyacetone phosphate 14. Increased expression of ALDOA has been found in a variety of cancers, such as lung cancer,15,16 pancreatic ductal adenocarcinoma,17 and hepatocellular carcinomas 18. Notably, decades ago, studies had identified an enhanced level of ALDOA in both cancer tissues and peripheral blood of patients with renal carcinoma 19,20.…”

Section: Introductionmentioning

confidence: 99%

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

Na¹,

Li²,

Xu³

et al. 2017

TCRM

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BackgroundAldolase A (ALDOA) is a glycolytic enzyme that drives the glycolytic metabolic pathway in mammalian cells. The overexpression of ALDOA was observed in a variety of cancers including clear-cell renal cell carcinoma (ccRCC). However, little was known about the clinicopathological significance and prognostic value of ALDOA in ccRCC patients.MethodsThe expression of ALDOA was detected using immunohistochemical staining in 162 formalin-fixed, paraffin-embedded ccRCC sections. Prognostic outcomes correlated with ALDOA were examined using Kaplan–Meier analysis and the Cox proportional hazards model.ResultsIn patients with ccRCC, increased cytoplasmic ALDOA expression was positively associated with tumor size (P=0.021), TNM stages (P=0.034), lymph node metastasis (P=0.020), and overall survival (OS) (P<0.001). Kaplan–Meier analysis showed that high cytoplasmic expression of ALDOA was associated with a statistically significant lower OS (P<0.001). Multivariate analysis demonstrated that ALDOA expression was an independent and significant prognostic factor (HR =3.561, 95% CI =1.715–7.396, P=0.001). ALDOA expression was not associated with significant prognostic deference in the subgroups of TNM stage I patients or pT1 patients.ConclusionOur results suggest that ALDOA expression is an independent prognostic factor for OS in patients with ccRCC.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Na¹,

Li²,

Xu³

et al. 2017

TCRM

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“…A recent report showed that ALDOA regulated C-myc to promote the growth and metastasis of pancreatic cancer cells [10]. To identify the mechanisms associated with snord105b in GC cells, we tested the expression levels of ALDOA and C-myc.…”

Section: Resultsmentioning

confidence: 99%

“…Du et al found that ALDOA might promote the progression of lung cancer through EMT [27]. Ji et al reported that ALDOA regulates C-myc to promote the growth and metastasis of pancreatic cancer cells [10]. First, we detected the expression level of ALDOA by western blotting.…”

Section: Discussionmentioning

confidence: 99%

C/D-Box Snord105b Promotes Tumorigenesis in Gastric Cancer via ALDOA/C-Myc Pathway

Zhang¹,

Zhao²,

Wu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Small nucleolar RNAs (snoRNAs) play an important role in carcinogenesis. In this study, we identified a C/D box snoRNA, snord105b, and further investigated the function and mechanism of the snord105b in gastric cancer (GC). Methods: The expression level of snord105b in GC tissures, sera and cell lines were detected by qRT-PCR. Cell viability was assessed using MTS assay. Transwell and wound healing assay were performed to evaluate migration and invasion, and protein expression was examined by western blotting. ChIRP and MS analysis was used to seek for the special binding protein of snord105b. Results: The snord105b was upregulated and associated with tumor size, differentiation, and pathological stage in GC. Snord105b affected proliferation, migration and invasion in multiple GC cell lines. The oncoqenic activity of snord105b was also confirmed with in vivo data. Mechanistically, snord105b specifically bound to ALDOA and affected C-myc, which plays a key role in carcinogenesis and tumor development. Conclusion: Snord105b appears to be a novel oncogene and is clinically and functionally involved in the development of GC. Targeting snord105b and its pathway may provide new biomarkers or potential treatments for patients with GC.

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Tumor Metabolism: Focused on Tumor Glycolysis, Progress, and Prospects in Cancer Therapy

Kumar

Singh

Sharma

et al. 2021

Burger's Medicinal Chemistry and Drug Discovery

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The metabolic reprogramming of cell is a well‐established clinical hallmark of cancer and accordingly has attracted significant attention from researchers in the field of drug discovery. The dependency of cancer cells toward altered “cancer metabolism” (CM) encouraged scientists to work to better understand their metabolic alteration and tumor microenvironment. In fact, the cellular energetics of cancer cells is significantly different from normal cells due to the high demand of energy and metabolites that are required for cancer cell growth and proliferation. A combination of identification of metabolic processes and detailed study of how oncogenic signaling pathways can modulate the metabolic processes might be useful to achieve the selective killing of cancer cells. Recently, several studies have confirmed that cancer metabolism plays a fundamental role in cancer progression and metastasis. Carbohydrate metabolism, particularly glucose metabolism in tumor cells, has received significant attention because rapidly growing cancer cells preferentially rely on the enhanced rate of tumor glycolytic process uncoupled with oxidative phosphorylation. Small molecules targeting tumor glycolysis hold promise for drug discovery and drug development in cancer therapeutics. In addition, it offers the development of new treatment options by synergizing potential glycolytic inhibitors with existing drugs. Therefore, this article includes recent updates on tumor glycolysis and small molecules that counteract tumor glycolysis.

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ALDOA functions as an oncogene in the highly metastatic pancreatic cancer

Cited by 121 publications

References 35 publications

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

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

C/D-Box Snord105b Promotes Tumorigenesis in Gastric Cancer via ALDOA/C-Myc Pathway

Tumor Metabolism: Focused on Tumor Glycolysis, Progress, and Prospects in Cancer Therapy

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