ERCC6L promotes the progression of hepatocellular carcinoma through activating PI3K/AKT and NF-κB signaling pathway

Han, Chunchun; Wang, Hengxiao; Yu, Xiqiao; Zhou, Shuping; Zhang, Yueying; Wang, Zhanhui; Huang, Shuhong

doi:10.1186/s12885-020-07367-2

Cited by 16 publications

(12 citation statements)

References 36 publications

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“…Given that tumorigenesis and metastasis of GC is a complicated process and is affected by numerous genetic changes [ 10 – 11 ], it is urgently required to determine novel molecular targets and the potential mechanisms responsible for this process. Remarkably, recent reports have identified ERCC6L as a critical mediator in the malignant biological behavior of various cancers [ 7 – 8 , 12 ]. For example, ERCC6L expression is increased in HCC tissue, which significantly correlates with poor clinical outcomes [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

“…For example, ERCC6L expression is increased in HCC tissue, which significantly correlates with poor clinical outcomes [ 7 ]. Furthermore, ERCC6L promotes tumor progression via the PI3K/AKT and NF-κB pathway in HCC [ 12 ]. In CRC, ERCC6L is significantly elevated in tumor tissues, and functions importantly in CRC cell growth, describing ERCC6L as a target for CRC [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

“…The mRNA level was evaluated according to the 2 -ΔΔCt method. Primers are summarized in Supplementary Table 1 [ 12 ].…”

Section: Methodsmentioning

confidence: 99%

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ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-κB signaling

Chen

Liu

Cao

2021

Aging

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ERCC6L has been reported to act as a potential oncogenic protein in various cancers. However, the role of ERCC6L in the progression of gastric cancer (GC) remains to be elucidated. Herein, we aimed to assess the clinical significance, the role, and the underlying mechanism of ERCC6L in GC progression. In this study, the mRNA and protein expression levels of ERCC6L were measured in GC specimens by quantitative real-time PCR (qRT-PCR), Western blot, and immunohistochemistry, and its clinical significance was assessed. The effect of ERCC6L overexpression or knockdown on GC cell growth, migration, and invasion was explored by functional experiments. Notably, the possible mechanisms underlying the action of ERCC6L were also investigated. We found that ERCC6L was upregulated in GC tissues, and its expression was associated with tumor size, clinical stage, and poor prognosis in GC patients. Besides, ERCC6L facilitated GC cell proliferation and metastasis in vitro and in vivo . Mechanically, ERCC6L modulated GC cell behavior via activation of NF-κB signaling. Our results indicated that ERCC6L played a critical role in GC progression and metastasis. In addition, ERCC6L promoted GC cell growth and metastasis via activation of NF-κB signaling, thus possibly providing a target for GC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-κB signaling

Chen

Liu

Cao

2021

Aging

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“…In addition, we found that PI3K-Akt and NF-kB signaling pathways were also signi cantly enriched. Studies have shown that NF-kB can act as downstream effectors of the PI3K-Akt pathway, and their abnormal activation is positively correlated with the malignant progression of HCC and leads to poor prognosis of HCC patients [35]. These enriched pathways suggest that PTGFRN may be involved in the progression of HCC at different stages.…”

Section: Correlation Of Ptgfrn Gene Expression On Survival and Multivariate Analysismentioning

confidence: 97%

Upregulation of PTGFRN in Hepatocellular Carcinoma Predicts Poor Prognosis: A Study Based on the TCGA Database

Tan¹,

Wu²,

Wang³

et al. 2021

Preprint

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Background. The importance of prostaglandin F2 receptor inhibitors (PTGFRN) in the progression of a variety of malignant tumors has been recognized in recent years. So far, no role of PTGFRN in hepatocellular carcinoma (HCC) has been reported. In this study, we focused on the possible mechanisms of PTGFRN in HCC based on the Cancer Genome Atlas (TCGA) data. Methods. The mRNA gene expression data of PTGFRN were downloaded from TCGA database to analyze the expression level of PTGFRN in HCC. According to the human protein atlas database, the expression difference of PTGFRN protein between HCC and adjacent tissues was verified. Wilcoxon signed-rank test and logistic regression were used to analyze the relationship between PTGFRN and clinicopathological characteristics. Kaplan Meier method and Cox proportional hazards model were used to explore the prognostic role of PTGFRN in HCC. The ROC curve was used to evaluate the diagnostic value of PTGFRN in HCC. Gene Set Enrichment Analysis (GSEA) was used to investigate the function of PTGFRN related Gene sets. Finally, obtain the co-expressed genes of PTGFRN through the cBioPortal database, and use the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) function enrichment analysis to further explore the role of PTGFRN in HCC regulated related pathways.Results. Analysis of mRNA expression data of 377 HCC patients showed that the expression of PTGFRN was up-regulated in HCC, which was confirmed by immunohistochemistry. The overexpression of PTGFRN was significantly correlated with clinical stage (P = 0.028) and histological grade (P = 0.027). High expression of PTGFRN was associated with poorer overall survival.. Meanwhile, multivariate Cox analysis showed that PTGFRN may be a potential independent risk factor for HCC. GSEA enrichment results showed that the up-regulated PTGFRN phenotype was concentrated in "endocytosis", "oocyte meiosis" and "ERBB signaling pathway". In addition, through the analysis of KEGG and GO pathways, we found that PTGFRN co-expressed genes are mainly involved in extracellular matrix tissue, epithelial-mesenchymal transition, cell adhesion and cell cycle, and PI3K-Akt/NF-kB signaling pathways.Conclusions. PTGFRN is highly expressed in HCC and can be used as an independent predictor of the clinical prognosis of HCC.

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“…The PI3K/AKT signaling pathway has important influence in pancreatic cancer metastasis (23). Recent studies indicate that NF-kB transcription factor might regulate the PI3K/AKT signaling pathway to trigger the metastasis-mediated effect (142). The authors show that RES reduces the expressions of p-AKT and p-NF-kB to suppress the PI3K/AKT/NF-kB pathway, inhibiting the invasion and migration of pancreatic cells as proved by suppressing the level of EMT-related markers (N-cadherin and vimentin) (23).…”

Section: Pancreatic Cancer and Cholangiocarcinomamentioning

confidence: 99%

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

et al. 2021

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Epithelial-to-mesenchymal transition (EMT), a complicated program through which polarized epithelial cells acquire motile mesothelial traits, is regulated by tumor microenvironment. EMT is involved in tumor progression, invasion and metastasis via reconstructing the cytoskeleton and degrading the tumor basement membrane. Accumulating evidence shows that resveratrol, as a non-flavonoid polyphenol, can reverse EMT and inhibit invasion and migration of human tumors via diverse mechanisms and signaling pathways. In the present review, we will summarize the detailed mechanisms and pathways by which resveratrol and its analogs (e.g. Triacetyl resveratrol, 3,5,4’-Trimethoxystilbene) might regulate the EMT process in cancer cells to better understand their potential as novel anti-tumor agents. Resveratrol can also reverse chemoresistance via EMT inhibition and improvement of the antiproliferative effects of conventional treatments. Therefore, resveratrol and its analogs have the potential to become novel adjunctive agents to inhibit cancer metastasis, which might be partly related to their blocking of the EMT process.

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ERCC6L promotes the progression of hepatocellular carcinoma through activating PI3K/AKT and NF-κB signaling pathway

Cited by 16 publications

References 36 publications

ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-κB signaling

ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-κB signaling

Upregulation of PTGFRN in Hepatocellular Carcinoma Predicts Poor Prognosis: A Study Based on the TCGA Database

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

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