PD-L1 Induces Epithelial‐Mesenchymal Transition in Nasopharyngeal Carcinoma Cells Through Activation of the PI3K/AKT Pathway

Fei, Zhenghua; Deng, Zhenmiao; Zhou, Lingyang; Li, Kejie; Xia, Xiaofang; Xie, Raoying

doi:10.3727/096504018x15446984186056

Cited by 28 publications

(44 citation statements)

References 27 publications

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“…6a). Numerous studies have reported that the PI3K/AKT pathway plays an important role in metastasis through the regulation of EMT [23][24][25]. Therefore, the PI3K inhibitor LY294002 [26][27][28][29] was used to detect the effect of the PI3K/AKT pathway on AGK-induced RCC proliferation and metastasis.…”

Section: Agk Promotes Rcc Proliferation and Metastasis Via The Pi3k/amentioning

confidence: 99%

Acylglycerol kinase promotes tumour growth and metastasis via activating the PI3K/AKT/GSK3β signalling pathway in renal cell carcinoma

Zhu

Zhong

et al. 2020

J Hematol Oncol

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Background: Clinically, the median survival in patients with metastatic renal cell carcinoma (RCC) was only 6-12 months and a 5-year survival rate of less than 20%. Therefore, an in-depth study of the molecular mechanisms involved in RCC is of great significance for improving the survival of patients with advanced RCC. Acylglycerol kinase (AGK) is a newly discovered lipid kinase that has been reported to be a potent oncogene that may be involved in the regulation of malignant progression in a variety of tumours. However, the expression and biological characteristics of the AGK gene in RCC remain unclear. Methods: AGK expression was quantified by quantitative real-time PCR, Western blotting and immunohistochemistry in RCC cell lines and paired patient tissues. Kaplan-Meier method and Cox proportional hazards models were used to evaluate the prognostic value of AGK in human RCC tissue samples. Chi-squared test was performed to analyse the correlation between AGK expression and the clinicopathological features. Stable overexpression and knockdown of AGK in RCC cells was constructed with lentivirus. The oncogenic effects of AGK in human RCC progression were investigated using assays of colony formation, anchorage-independent growth, EdU assay, cell cycle analysis, wound-healing, trans-well analysis and xenograft tumour model. GSEA and KEGG analysis were conducted to detect the potential pathway of AGK involved in RCC. These results were further confirmed using the luciferase reporter assays, immunofluorescence and in vivo experiments. Results: AGK expression is significantly elevated in RCC and closely related to the malignant development and poor prognosis in RCC patients. By in vitro and in vivo experiments, AGK was shown to enhance the proliferation of RCC cells by promoting the transition from the G1 phase to the S phase in the cell cycle and to enhance the migration and invasion by promoting epithelial-mesenchymal transition. By activating the PI3K/AKT/GSK3β signalling pathway in RCC, AGK can increase nuclear accumulation of β-catenin, which further upregulated TCF/LEF transcription factor activity. Conclusions: AGK promotes the progression of RCC via activating the PI3K/AKT/GSK3β signalling pathway and might be a potential target for the further research of RCC.

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Section: Agk Promotes Rcc Proliferation and Metastasis Via The Pi3k/amentioning

confidence: 99%

Acylglycerol kinase promotes tumour growth and metastasis via activating the PI3K/AKT/GSK3β signalling pathway in renal cell carcinoma

Zhu

Zhong

et al. 2020

J Hematol Oncol

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“…Similarly, synthetic peptides that either target PD-L1 degradation or post-translational modifications have shown a strong efficiency in animal studies, which may serve as a novel therapy for cancer treatment (351, 365). Notably, this kind of therapy that directly targets PD-L1 is of great significance and may be more effective as compared with blockade of PD-1/PD-L1 axis due to PD-1-independent functions of PD-L1 in the promotion of malignant phenotypes and drug resistance (367, 368). Altogether, an extensive understanding of the mechanisms by which PD-L1 is governed will help us to reach a comprehensive evaluation of PD-1/PD-L1 targeting therapy, and further potentiate the efficacy and expand the usage of this kind of cancer therapy via patient selection and rational combination with other antineoplastic agents, as well as develop new effective strategies for cancer immunotherapy.…”

Section: Discussionmentioning

confidence: 99%

Recent Findings in the Regulation of Programmed Death Ligand 1 Expression

et al. 2019

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With the recent approvals for the application of monoclonal antibodies that target the well-characterized immune checkpoints, immune therapy shows great potential against both solid and hematologic tumors. The use of these therapeutic monoclonal antibodies elicits inspiring clinical results with durable objective responses and improvements in overall survival. Agents targeting programmed cell death protein 1 (PD-1; also known as PDCD1) and its ligand (PD-L1) achieve a great success in immune checkpoints therapy. However, the majority of patients fail to respond to PD-1/PD-L1 axis inhibitors. Expression of PD-L1 on the membrane of tumor and immune cells has been shown to be associated with enhanced objective response rates to PD-1/PD-L1 inhibition. Thus, an improved understanding of how PD-L1 expression is regulated will enable us to better define its role as a predictive marker. In this review, we summarize recent findings in the regulation of PD-L1 expression.

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“…Furthermore, CD163 is considered the most speci c marker of TAMS, involved in the occurrence, development, migration, angiogenesis, EMT, etc., of GBM [42,43]. PD-L1 is the focus of current immunotherapy research, the study found that its expression is closely related to EMT [44,45], and EMT is the focus of current cancer resistance research [46,47]. But no research has been done to explore the causes of individualization of patient therapy through their relationship.…”

Section: Discussionmentioning

confidence: 99%

The High Expression of CD276/HAVCR2 and CD163 is an Adverse Immune Subtype of Glioblastoma and is Closely Related to Epithelial-Mesenchymal Transition

Hou

Zhou

Fan

et al. 2020

Preprint

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Background Glioblastoma (GBM) is one of the most malignant tumors that can afflict the central nervous system. Previous studies have observed that there are individual differences in the treatment response of immune checkpoint inhibitors in glioblastoma. This study’s aim is to ascertain the factors that may affect the efficacy of immunosuppressant therapy. Methods The clinical data of this study were obtained from a public database. Then, the data was analyzed and processed by R software and corresponding R package. To verify the results of the analysis, information was gathered from 89 GBM patients in our hospital and thereafter the corresponding paraffin sections were stained and quantitatively analyzed by immunohistochemistry. Results From the analysis, it was observed that both CD276 and HAVCR2 were significantly overexpressed in GBM and could be associated with patient prognosis. The analysis of single cell RNA sequencing data and GBM data analysis found an immune subtype with poor prognosis. Further analysis found that the high expression of CD276, HAVCR2 and CD163 was closely related to epithelial-mesenchymal transition (EMT) and could affect the patient prognosis of PD-L1 high expression. GSVA enrichment analysis showed that CD276, HAVCR2 and CD163 might induce EMT by JAK-STAT3 signaling pathway, and RUNX1 and IKZF1 might be transcription factors that regulate CD276/HAVCR2 high expression. Conclusions We found an immune subtype with poor prognosis of GBM, the high expression of CD276, HAVCR2 and CD163 with EMT are closely related and may be one of the factors affecting the efficacy of Anti-PD-L1.

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PD-L1 Induces Epithelial‐Mesenchymal Transition in Nasopharyngeal Carcinoma Cells Through Activation of the PI3K/AKT Pathway

Cited by 28 publications

References 27 publications

Acylglycerol kinase promotes tumour growth and metastasis via activating the PI3K/AKT/GSK3β signalling pathway in renal cell carcinoma

Acylglycerol kinase promotes tumour growth and metastasis via activating the PI3K/AKT/GSK3β signalling pathway in renal cell carcinoma

Recent Findings in the Regulation of Programmed Death Ligand 1 Expression

The High Expression of CD276/HAVCR2 and CD163 is an Adverse Immune Subtype of Glioblastoma and is Closely Related to Epithelial-Mesenchymal Transition

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