Targeting eukaryotic protein translation in mesothelioma

Kratzke, Robert A.

doi:10.21037/tlcr.2017.06.07

Cited by 5 publications

(5 citation statements)

References 29 publications

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“…Consistent with this model, PAIP1 knockdown downregulates CCND1 and CCND2 expression in HCC cells, thereby restricting cyclin D/CDK activity and producing the observed anti-malignant effects. Based on Kratze et al's proposed model [30], we speculate that PAIP1 expression in HCC cells promotes eIF4G hyper-activation, thereby promoting preferential translation of CCND1 and CCND2 transcripts.…”

Section: Discussionmentioning

confidence: 78%

“…Although more research is required to reveal the underlying mechanism of PAIP1 in tumorigenesis, there is a substantial body of evidence linking dysregulations in PAIP1-associated translational initiation factors with oncogenesis [29]. Kratze et al has reported that many malignancies display hyper-activation of eIF4 proteins (i.e., eIF4A, eIF4E, eIF4G, and 4E-BP proteins), resulting in enhanced binding to the 5' cap and preferential translation of cancer-associated genes, including cyclin D1, c-myc, and ornithine decarboxylase [30]. As PAIP1 stabilizes PABP's interaction with eIF4G [7], the PAIP1 upregulation in HCC cells observed here may promote the translation of oncogenic mRNAs through promoting eIF4G hyperactivation.…”

Section: Discussionmentioning

confidence: 99%

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PAIP1 is a Novel Oncogene in Human Hepatocellular Carcinoma

Zhang

Chen

2022

Preprint

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Background: Poly(A)-binding protein interacting protein 1 (PAIP1) is a translational initiation regulatory factor that has been reported as oncogene in multiple malignant diseases. However, its role in hepatocellular carcinoma (HCC) and the potential mechanisms underlying tumor progression have not been explored. Methods: PAIP1 expression level in HCC cell lines were detected by real-time PCR and western blotting. When PAIP1 was knocked down, the proliferation and colony formation of HCC cell lines were detected by MTT and colony formation assay. The apoptosis and cell cycle were detected by flow cytometry. The volume and growth rate of the xenograft tumors were observed. The potential mechanism of PAIP1 in HCC cells was analyzed by miRNA Microarray Analysis and TargetScan analysis. Results: PAIP1 is significantly upregulated in HCC cell lines. PAIP1 knockdown dramatically inhibits cell proliferation and colony formation, induces apoptosis and alters the cell cycle profile by increasing the G2/M cell percentage. Moreover, PAIP1 knockdown significantly reduces xenograft tumorigenesis in a murine transplantation model. Bioinformatics and immunoblotting analysis reveal PAIP1 knockdown dysregulates cyclin D pathway-related proteins. Conclusion: PAIP1 functions an oncogenic role in hepatocellular carcinoma.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

PAIP1 is a Novel Oncogene in Human Hepatocellular Carcinoma

Zhang

Chen

2022

Preprint

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show abstract

“…Consistently,l PAIP1 knockdown downregulates CCND1 and CCND2 expression in HCC cells, thereby restricting cyclin D/CDK activity and producing the observed anti-malignant effects. Based on Kratze et al’s proposed model [ 29 ], we speculate that PAIP1 expression in HCC cells promotes eIF4G hyper-activation, thereby promoting preferential translation of CCND1 and CCND2 transcripts.…”

Section: Discussionmentioning

confidence: 82%

“…Although more research is required to reveal the underlying mechanism of PAIP1 in tumorigenesis, there is a substantial body of evidence linking dysregulations in PAIP1-associated translational initiation factors with oncogenesis [ 28 ]. Kratze et al has reported that many malignancies display hyper-activation of eIF4 proteins (i.e., eIF4A, eIF4E, eIF4G, and 4E-BP proteins), resulting in enhanced binding to the 5’ cap and preferential translation of cancer-associated genes, including cyclin D1, c-myc, and ornithine decarboxylase [ 29 ]. As PAIP1 stabilizes PABP’s interaction with eIF4G [ 6 ], the PAIP1 upregulation in HCC cells observed here may promote the translation of oncogenic mRNAs by promoting eIF4G hyper-activation.…”

Section: Discussionmentioning

confidence: 99%

PAIP1 is a novel oncogene in human hepatocellular carcinoma

Zhang

Chen

2022

Discov Onc

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Background Poly(A)-binding protein interacting protein 1 (PAIP1) is a translational initiation regulatory factor that has been reported as oncogene in multiple malignant diseases. However, its role in hepatocellular carcinoma (HCC) and the potential mechanisms have not been explored. Methods PAIP1 expression level in HCC cell lines were detected by real-time quantitative PCR and western blotting. The proliferation and colony formation of HCC cell lines were detected by MTT and colony formation assay. The apoptosis and cell cycle were detected by flow cytometry. The volume and growth rate of the xenograft tumors were observed. The potential mechanism of PAIP1 was analyzed by miRNA Microarray Analysis and TargetScan analysis. Results PAIP1 is significantly upregulated in HCC cell lines. PAIP1 knockdown dramatically inhibits cell proliferation and colony formation, induces apoptosis and alters the cell cycle distribution by increasing the G2/M cell percentage. Moreover, PAIP1 knockdown significantly reduces tumorigenesis in a murine transplantation model. Bioinformatics and immunoblotting analysis reveal that PAIP1 knockdown dysregulates cyclin D pathway-related proteins. Conclusion PAIP1 plays an oncogenic role in hepatocellular carcinoma.

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“…Our results reveal that, besides the previously described elongation factors, initiation factors such as EIF3G and EIF-4II are also involved in lung cancer. To date, these factors have only been attributed to other cancers, such as mesothelioma [ 188 ] and colorectal cancers [ 189 ].…”

Section: Discussionmentioning

confidence: 99%

Application of two-dimensional difference gel electrophoresis to identify protein changes between center, margin, and adjacent non-tumor tissues obtained from non-small-cell lung cancer with adenocarcinoma or squamous cell carcinoma subtype

et al. 2022

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Lung cancer is responsible for the most cancer-related mortality worldwide and the mechanism of its development is poorly understood. Proteomics has become a powerful tool offering vital knowledge related to cancer development. Using a two-dimensional difference gel electrophoresis (2D-DIGE) approach, we sought to compare tissue samples from non-small-cell lung cancer (NSCLC) patients taken from the tumor center and tumor margin. Two subtypes of NSCLC, adenocarcinoma (ADC) and squamous cell carcinoma (SCC) were compared. Data are available via ProteomeXchange with identifier PXD032736 and PXD032962 for ADC and SCC, respectively. For ADC proteins, 26 significant canonical pathways were identified, including Rho signaling pathways, a semaphorin neuronal repulsive signaling pathway, and epithelial adherens junction signaling. For SCC proteins, nine significant canonical pathways were identified, including hypoxia-inducible factor-1α signaling, thyroid hormone biosynthesis, and phagosome maturation. Proteins differentiating the tumor center and tumor margin were linked to cancer invasion and progression, including cell migration, adhesion and invasion, cytoskeletal structure, protein folding, anaerobic metabolism, tumor angiogenesis, EMC transition, epithelial adherens junctions, and inflammatory responses. In conclusion, we identified several proteins that are important for the better characterization of tumor development and molecular specificity of both lung cancer subtypes. We also identified proteins that may be important as biomarkers and/or targets for anticancer therapy.

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Targeting eukaryotic protein translation in mesothelioma

Cited by 5 publications

References 29 publications

PAIP1 is a Novel Oncogene in Human Hepatocellular Carcinoma

PAIP1 is a Novel Oncogene in Human Hepatocellular Carcinoma

PAIP1 is a novel oncogene in human hepatocellular carcinoma

Application of two-dimensional difference gel electrophoresis to identify protein changes between center, margin, and adjacent non-tumor tissues obtained from non-small-cell lung cancer with adenocarcinoma or squamous cell carcinoma subtype

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