Study of the G Protein Nucleolar 2 Value in Liver Hepatocellular Carcinoma Treatment and Prognosis

Dong, Yiwei; Cai, Qianqian; Fu, Lisheng; Liu, Haojie; Ma, Mingzhe; Wu, Xingzhong

doi:10.1155/2021/4873678

Cited by 5 publications

(3 citation statements)

References 30 publications

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“…HCC frequently coexists with chronic liver conditions like cirrhosis, which can exacerbate the progression of HCC. This concomitance underscores the complex nature of HCC’s pathogenesis and highlights the importance of early intervention and comprehensive management of underlying liver conditions to mitigate the severity of HCC ( 17 , 18 ). Currently, the intricate mechanisms underpinning HCC are not fully understood.…”

Section: Discussionmentioning

confidence: 93%

Propofol regulates the progression of hepatocellular carcinoma via the POLR2L/TGF-β signaling pathway

Chen,

Xu,

et al. 2024

Transl Cancer Res

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Background Hepatocellular carcinoma (HCC) is a malignant tumor with high morbidity and mortality. Propofol has been reported to modulate tumorigenesis in HCC; the aim of this study was to investigate the effect of the interaction of propofol with POLR2L on HCC tumor progression in HCC. Methods The propofol-related GSE101724 dataset was analyzed using weighted gene co-expression network analysis (WGCNA) and differentially expressed genes (DEGs) to identify overlapping genes. Key genes were selected from The Cancer Genome Atlas-liver hepatocellular carcinoma (TCGA-LIHC)-DEGs for prognostic analysis. The impact of POLR2L on LIHC patient survival was assessed, followed by in vitro experiments to validated its effects on HCC cell behavior and signaling pathways. Results Fourteen overlapping genes were identified in the turquoise module (highest correlation) of up-regulated DEGs and GSE101724. Further analysis obtained 11 key overlapping genes from 14 overlapping genes and TCGA-LIHC-DEGs, among which HSPE1 and POLR2L showed significant prognostic correlation. Patients with LIHC have a worse chance of surviving when their POLR2L expression is elevated. Knockdown POLR2L significantly inhibited the proliferation, invasion, and migration of HCC cell lines. Downregulation of POLR2L was accompanied by induced apoptosis, cell cycle arrest, and modulation of the expression of apoptosis-related genes. Propofol was found to downregulate POLR2L expression, inhibiting cell proliferation and growth. Further, it was shown that propofol controlled the development of HCC by influencing the POLR2L/TGF-β signaling loop. Conclusions The results validated the predictive relevance of POLR2L in HCC and emphasized that propofol can regulate HCC progression through the POLR2L/TGF-β signaling pathway.

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Section: Discussionmentioning

confidence: 93%

Propofol regulates the progression of hepatocellular carcinoma via the POLR2L/TGF-β signaling pathway

Chen,

Xu,

et al. 2024

Transl Cancer Res

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“…The GNL2 family encompasses two members, namely GNL3 (nucleoprotein) and GNL3-like (GNL3L) ( 36 ). While GNL3L functions as the vertebrate equivalent of the nucleostemin, GNL2 has a unique presence across both vertebrate and invertebrate species ( 37 ). The contribution of GNL2 to various cancers has been previously highlighted in the literature.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic role of RNA-binding protein GNL2 in glioma: Promotion of tumor development through enhancing protein synthesis

Yang,

2024

Oncol Lett

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RNA-binding proteins (RBPs) are aberrantly expressed in various diseases, including glioma. In the present study, the role and mechanism of RBPs in glioma were investigated. Differentially expressed genes (DEGs) in glioma were screened from public databases and overlapping genes between DEGs and RBPs were selected in a bioinformatics analysis to identify the hub gene. Next, evaluation of expression, survival analysis and cell experiments were performed to examine the impact of the hub gene on glioma. Through bioinformatics analysis, G protein nucleolar 2 (GNL2), programmed cell death 11 (PDCD11) and ribosomal protein S6 (RPS6) were identified as potential biomarkers in glioma prognosis and GNL2 was chosen as the hub gene for further investigation. GNL2 was increased in glioma tissues and related to poor survival outcomes. Cell experiments revealed that GNL2 knockdown inhibited glioma cell growth, migration and invasion. In addition, GNL2 was found to affect the overall protein synthesis of ribosomal protein L11 in glioma cells. In conclusion, GNL2, PDCD11 and RPS6 may serve as potential biomarkers in glioma prognosis. Importantly, GNL2 acts as an oncogene in glioma and it enhances protein synthesis to promote the development of brain glioma.

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“…As a protein-encoding gene, G protein nucleolar 2 (GNL2) goes by several other names, including NGP1 , Nog2 , Nug2 , Ngp-1 , and HUMAUANTIG . Dong et al ( 59 ) reported that HCC patients with high GNL2 expression had lower survival rates, and in vitro knockdown investigations demonstrated that decreasing GNL2 using siRNA inhibited HCC cell proliferation, migration, and invasion capabilities. Consequently, the model may be utilized to assess the prognosis of HCC.…”

Section: Discussionmentioning

confidence: 99%

Identification of cuproptosis and ferroptosis-related subgroups and development of a signature for predicting prognosis and tumor microenvironment landscape in hepatocellular carcinoma

Yang,

Ma,

Hui

et al. 2023

Transl Cancer Res

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Background Ferroptosis and cuproptosis play a crucial role in the progression and dissemination of hepatocellular carcinoma (HCC). The primary objective of this study was to develop a unique scoring system for predicting the prognosis and immunological landscape of HCC based on ferroptosis-related genes (FRGs) and cuproptosis-related genes (CRGs). Methods As the training cohort, we assembled a novel HCC cohort by merging gene expression data and clinical data from The Cancer Genome Atlas (TCGA) database, and Gene Expression Omnibus (GEO) database. The validation cohort consisted of 230 HCC cases taken from the International Cancer Genome Consortium (ICGC) database. Multiple genomic characteristics, such as tumor mutation burden (TMB), and copy number variations were analyzed concurrently. On the basis of the expression of CRGs and FRGs, patients were classified into cuproptosis and ferroptosis subtypes. Then, we constructed a risk model using least absolute shrinkage and selection operator (LASSO) analysis and Cox regression analysis based on ferroptosis and cuproptosis-related differentially expressed genes (DEGs). Patients were separated into two groups according to median risk score. We compared the immunophenotype, tumor microenvironment (TME), cancer stem cell index, and treatment sensitivity of two groups. Results Three subtypes of ferroptosis and two subtypes of cuproptosis were identified among the patients. A greater likelihood of survival (P<0.05) was expected for patients in FRGcluster B and CRGcluster B. After that, a confirmed risk signature for ferroptosis and cuproptosis was developed and tested. Patients in the low-risk group had significantly higher survival rates than those in the high-risk group, according to our study (P<0.001). There was also a strong correlation between the signature and other variables including immunophenoscore, TMB, cancer stem cell index, immunological checkpoint genes, and sensitivity to chemotherapeutics. Conclusions Through this comprehensive research, we identified a unique risk signature associated with HCC patients’ treatment status and prognosis. Our findings highlight FRGs’ and CRGs’ significance in clinical practice and imply ferroptosis and cuproptosis may be therapeutic targets for HCC patients.

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Study of the G Protein Nucleolar 2 Value in Liver Hepatocellular Carcinoma Treatment and Prognosis

Cited by 5 publications

References 30 publications

Propofol regulates the progression of hepatocellular carcinoma via the POLR2L/TGF-β signaling pathway

Propofol regulates the progression of hepatocellular carcinoma via the POLR2L/TGF-β signaling pathway

Oncogenic role of RNA-binding protein GNL2 in glioma: Promotion of tumor development through enhancing protein synthesis

Identification of cuproptosis and ferroptosis-related subgroups and development of a signature for predicting prognosis and tumor microenvironment landscape in hepatocellular carcinoma

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