The value of a metabolic reprogramming-related gene signature for pancreatic adenocarcinoma prognosis prediction

Tan, Zhen; Lei, Yubin; Xu, Jin; Shi, Si; Hua, Jie; Zhang, Bo; Meng, Qingcai; Liu, Jiang; Zhang, Yiyin; Wei, Miaoyan; Yu, Xianjun; Liang, Chen

doi:10.18632/aging.104134

Cited by 18 publications

(26 citation statements)

References 28 publications

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“…For example, previous researches reported that ENO3 was highly expressed in STK11 mutant lung cancer, colorectal cancer, and its ectopic expression correlated with a worse outcome of patients by bioinformatic analysis ( Park et al, 2019 ; Zhu et al, 2021 ). However, the results were converse in pancreatic carcinoma and HCC ( Liu et al, 2019 ; Tan et al, 2020 ). Based on results derived from the TCGA database, ICGC database, and clinical samples, we found that ENO3 was notably downregulated in human HCC samples in contrast to the neighboring normal tissue.…”

Section: Discussionmentioning

confidence: 91%

“…Apart from these, ENO3 has also been involved in various tumors, though the results are contradictory. For example, ENO3 is up-regulated in STK11 mutant pulmonary carcinoma ( Park et al, 2019 ) and colorectal carcinoma ( Xiaohang et al, 2020 ; Zhu et al, 2021 ), while down-regulated in pancreatic cancer ( Tan et al, 2020 ) and hepatocellular carcinomas ( Liu et al, 2019 ). Interestingly, down-regulation of ENO3 is also found in the activated human hepatic stellate cells, which can induce liver fibrosis and cirrhosis ( Zhong et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

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ENO3 Inhibits Growth and Metastasis of Hepatocellular Carcinoma via Wnt/β-Catenin Signaling Pathway

Cui

Guo²,

Zhang³

et al. 2021

Front. Cell Dev. Biol.

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β-enolase (ENO3) is a metalloenzyme that functions during glycolysis and has been revealed ectopic expression in different cancers. However, the function and underlying modulatory mechanisms of ENO3 in hepatocellular carcinoma (HCC) are still elusive. Here, we discovered that ENO3 was remarkably down-regulated in human HCC tissue in contrast to those in noncancerous tissue. Moreover, low expression of ENO3 was related to the poor prognosis of HCC patients. Overexpression of ENO3 suppressed proliferative, migratory, and invasive abilities of HCC cells both in vitro and in vivo, whereas knocking down ENO3 led to the opposite effect. In addition, we revealed that ENO3 repressed the epithelial-mesenchymal transition (EMT) process with its biomarker variations. Mechanistic research unveiled that ENO3 suppressed the Wnt/β-catenin signal, which subsequently modulated the transcription of its target genes associated with the proliferation and metastasis capacity of HCC cells. Taken together, our study uncovered that ENO3 acted as a tumor inhibitor in HCC development and implied ENO3 as a promising candidate for HCC treatment.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

ENO3 Inhibits Growth and Metastasis of Hepatocellular Carcinoma via Wnt/β-Catenin Signaling Pathway

Cui

Guo²,

Zhang³

et al. 2021

Front. Cell Dev. Biol.

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“…However, the authors did not conduct further studies on the expression of numerous immune checkpoints to explore whether risk stratification is a guide to immunosuppressive therapy. Tan’s work ( 31 ) was more concerned with metabolic reprogramming, which is one of the hallmarks of cancer, including enhanced lipid metabolism and glycolysis ( 32 , 33 ), and therefore established a three-gene prognostic signature based on genes related to glycolysis and lipid metabolism. The clinical therapeutic value of targeting the signature gene c-Met for oncogenesis and metastasis and the association of CD36 with PC resistance to gemcitabine were proposed.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Value and Correlation With Tumor Immune Infiltration of a Novel Metabolism-Related Gene Signature in Pancreatic Cancer

Chen

Zeng

et al. 2022

Front. Oncol.

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BackgroundEnergy metabolism has been considered as one of the novel features of neoplasms. This study aimed to establish the prognostic signature for pancreatic cancer (PC) based on metabolism-related genes (MRGs).MethodsWe obtained MRGs from the Molecular Signatures Database (MSigDB) and gene sequence data in the Cancer Genome Atlas (TCGA) databases. Then, differentially expressed MRGs (DE-MRGs) were identified utilizing the R software. We built the prognostic model via multivariate Cox regression. Moreover, external validation of the prognostic signature was also performed. Nomogram was created to predict the overall survival (OS). Next, this study analyzed the prognostic value, clinical relationship, and metabolism-related signaling pathways of the prognostic signature. The role in tumor infiltration was further evaluated. Eventually, the expression level of the three MRGs along with the function of NT5E was validated.ResultsTwenty-two MRGs were chosen, eight of which were identified to be most significantly correlated with the prognosis of PC. Meanwhile, a 3-MRG prognostic signature was established, and we verified this prognostic model in two separate external cohorts. What is more, the nomogram was used to predict 1-/2-/3-year OS of PC patients. In addition, the immune cell infiltration and expression of immune checkpoint were significantly influenced by the risk score. Finally, three MRGs were highly expressed in PC cell lines, and NT5E was associated with the proliferation and migration ability of PC.ConclusionTo sum up, the study established and validated a 3-MRG prognostic signature for PC, and the signature could be utilized to predict the prognosis and assist the individualized clinical management of patients with PC.

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“…Advances in gene chip and high-throughput sequencing have enabled novel development of reliable prognostic models for PDAC patients. To our surprise, there are many models that predict overall survival ( Feng et al, 2020 ; Tan et al, 2020 ; Wu et al, 2020a ; Xu et al, 2021 ), but few that predict RFS. Meanwhile, few studies have analyzed ferroptosis-related genes expression profiles to construct a risk prediction model.…”

Section: Discussionmentioning

confidence: 99%

A Novel Ferroptosis-Related Gene Signature Predicts Recurrence in Patients With Pancreatic Ductal Adenocarcinoma

Feng

Chen

et al. 2021

Front. Mol. Biosci.

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Background: Recurrence after surgery is largely responsible for the extremely poor outcomes for patients with pancreatic ductal adenocarcinoma (PDAC). Ferroptosis is implicated in chemotherapy sensitivity and tumor recurrence, we aimed to find out survival-associated ferroptosis-related genes and use them to build a practical risk model with the purpose to predict PDAC recurrence.Methods: Univariate Cox regression analysis was conducted to obtain prognostic ferroptosis-related genes in The Cancer Genome Atlas (TCGA, N = 140) cohort. Multivariate Cox regression analysis was employed to construct a reliable and credible gene signature. The prognostic performance was verified in a MTAB-6134 (N = 286) validation cohort and a PACA-CA (N = 181) validation cohort. The stability of the signature was tested in TCGA and MTAB-6134 cohorts by ROC analyses. Pathway enrichment analysis was adopted to preliminary illuminate the biological relevance of the gene signature.Results: Univariate and multivariate Cox regression analyses identified a 5-gene signature that contained CAV1, DDIT4, SLC40A1, SRXN1 and TFAP2C. The signature could efficaciously stratify PDAC patients with different recurrence-free survival (RFS), both in the training and validation cohorts. Results of subgroup receiver operating characteristic curve (ROC) analyses confirmed the stability and the independence of this signature. Our signature outperformed clinical indicators and previous reported models in predicting RFS. Moreover, the signature was found to be closely associated with several cancer-related and drug response pathways.Conclusion: This study developed a precise and concise prognostic model with the clinical implication in predicting PDAC recurrence. These findings may facilitate individual management of postoperative recurrence in patients with PDAC.

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The value of a metabolic reprogramming-related gene signature for pancreatic adenocarcinoma prognosis prediction

Cited by 18 publications

References 28 publications

ENO3 Inhibits Growth and Metastasis of Hepatocellular Carcinoma via Wnt/β-Catenin Signaling Pathway

ENO3 Inhibits Growth and Metastasis of Hepatocellular Carcinoma via Wnt/β-Catenin Signaling Pathway

Prognostic Value and Correlation With Tumor Immune Infiltration of a Novel Metabolism-Related Gene Signature in Pancreatic Cancer

A Novel Ferroptosis-Related Gene Signature Predicts Recurrence in Patients With Pancreatic Ductal Adenocarcinoma

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