EFLDO sensitizes liver cancer cells to TNFSF10‑induced apoptosis in a p53‑dependent manner

Qu, Yanbo; Liao, Zhi‐Xin; Wang, Xinzhu; Zhang, Jing; Liu, Chao

doi:10.3892/mmr.2019.10046

Cited by 9 publications

(8 citation statements)

References 28 publications

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“…Because of the multifaceted effect of CXCL10 on the biological behavior of various cancers, it is challenging to utilize CXCL10 as a therapy target. TNFSF10, the superfamily member 10 of tumor necrosis factor (TNF), acts in an antitumor capacity by inducing cancer cell apoptosis while interacting with the corresponding receptor ( Qu et al, 2019 ). However, De Looff et al noted that complex TME–tumor biological interactions would impede the tumor reduction effect of therapeutic TNFSF10 receptor agonists ( de Looff et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

An Inflammatory Response-Related Gene Signature Reveals Distinct Survival Outcome and Tumor Microenvironment Characterization in Pancreatic Cancer

Xie

Huang

et al. 2022

Front. Mol. Biosci.

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Background: Desmoplasia or rich fibrotic stroma is a typical property of pancreatic cancer (PC), with a significant impact on tumor progression, metastasis, and chemotherapy response. Unusual inflammatory responses are considered to induce fibrosis of tissue, but the expression and clinical significance of inflammatory response-related genes in PC have not been clearly elucidated.Methods: Prognosis-related differentially expressed genes (DEGs) between tumor and normal tissues were identified by comparing the transcriptome data of PC samples based on The Cancer Genome Atlas (TCGA) portal and the Genotype Tissue Expression (GTEx) databases. Samples from the ArrayExpress database were used as an external validation cohort.Results: A total of 27 inflammatory response-related DEGs in PC were identified. Least absolute shrinkage and selection operator (LASSO) analysis revealed three core genes that served as an inflammatory response gene signature (IRGS), and a risk score was calculated. The diagnostic accuracy of the IRGS was validated in the training (n = 176) and validation (n = 288) cohorts, which reliably predicted the overall survival (OS) and disease-free survival (DFS) of patients with PC. Furthermore, multivariate analysis identified the risk score as an independent risk factor for OS and DFS. The comprehensive results suggested that a high IRGS score was correlated with decreased CD8+ T-cell infiltration, increased M2 macrophage infiltration, increased occurrence of stroma-activated molecular subtype and hypoxia, enriched myofibroblast-related signaling pathways, and greater benefit from gemcitabine.Conclusion: The IRGS was able to promisingly distinguish the prognosis, the tumor microenvironment characteristics, and the benefit from chemotherapy for PC.

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Section: Discussionmentioning

confidence: 99%

An Inflammatory Response-Related Gene Signature Reveals Distinct Survival Outcome and Tumor Microenvironment Characterization in Pancreatic Cancer

Xie

Huang

et al. 2022

Front. Mol. Biosci.

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“…Previous study has suggested SMAD7 can induce growth and inhibit apoptosis in colon adenocarcinoma cells and acts as a tumor promoter [35], indicating that miR-581-mediated apoptosis might be SMAD7/TGFβ-pathway-independent. Moreover, in the results of miR-581 target genes, TNFSF10 [36,37], HMGA2 [38], CEACAM1 [39,40], and mTOR [41] have been reported to be involved in proliferation and apoptosis in a number of cancers. There is a strong possibility that miR-581 regulates CRC proliferation and apoptosis by targeting these genes.…”

Section: Discussionmentioning

confidence: 99%

MiR-581/SMAD7 Axis Contributes to Colorectal Cancer Metastasis: A Bioinformatic and Experimental Validation-Based Study

Zhao

Liu

Yan

et al. 2020

IJMS

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Metastasis is a well-known poor prognostic factor and primary cause of mortality in patients with colorectal cancer (CRC). Recently, with the progress of high through-put sequencing, aberrantly expressed non-coding RNAs (ncRNAs) were found to participate in the initiation and development of cancer. However, the mechanisms of ncRNA-mediated regulation of metastasis in CRC remain largely unknown. In this study, we systematically analyzed the expression network of microRNAs (miRNAs) and genes in CRC metastasis using bioinformatics, and discovered that the miR-581/SMAD7 axis could be a potential factor that drives CRC metastasis. A dual luciferase report assay and protein analysis confirmed the binding relationship between miR-581 and SMAD7. Further functional assays revealed that miR-581 inhibition could suppress cell proliferation and induce apoptosis in SW480 cells. Up-regulation or down-regulation of miR-581 could both affect cell invasion capacity and modulate epithelial to mesenchymal transition (EMT) via a SMAD7/TGFβ signaling pathway. In conclusion, our findings elucidated that miR-581/SMAD7 could be essential for CRC metastasis, and may serve as a potential therapeutic target for CRC patients.

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“…The exogenous apoptotic pathway primarily consists of a combination of death receptors and ligands leading to the receptor multimerization, in which TNFSF10 acts as a ligand that binds to death receptors DR4 and DR5 and activates caspase-8 to trigger the apoptotic cascade reaction (42). The B-cell lymphoma 2 (BCL2) family regulates the permeability of the mitochondrial outer membrane by polymerizing and depolymerizing with the components in this family (43).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, gga-miR-29b-3p was found to inhibit the proliferation of an MDV-derived chicken lymphocyte line, MDCC-MSB1, and the decrease in cell proliferation rate resulted from an elevated number of apoptotic cells; the apoptotic pathways included exogenous pathway triggered by death receptors and endogenous pathway triggered by mitochondria ( 41 ). The exogenous apoptotic pathway primarily consists of a combination of death receptors and ligands leading to the receptor multimerization, in which TNFSF10 acts as a ligand that binds to death receptors DR4 and DR5 and activates caspase-8 to trigger the apoptotic cascade reaction ( 42 ). The B-cell lymphoma 2 (BCL2) family regulates the permeability of the mitochondrial outer membrane by polymerizing and depolymerizing with the components in this family ( 43 ).…”

Section: Discussionunclassified

Role of gga-miR-29b-3p in suppressing the proliferation, invasion and migration of MSB1 Marek’s disease tumor cells by the targeting of the DNMT3B gene

Han¹,

Lian²,

Ren³

et al. 2022

Ann Transl Med

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Background: Marek's disease (MD), a class II infectious, lymphoproliferative disease that mainly afflicts poultry, has been shown to cause wasting, limb paralysis, and often acute death. It is a neoplastic disease caused by a cell-binding herpesvirus that leads to the formation of tumors in various organs and tissues. Our previous reports have found that the microRNA, gga-miR-29b-3p, showed abnormal expression in MD lymphoma. However, it remains unknown whether gga-miR-29b-3p affects MD tumorigenesis. Methods:The MD tumor cell line MSB1 was chosen to analyze the characteristics of gga-miR-29b-3p in tumors. Cell proliferation and migration were assessed by Cell Counting Kit-8 (CCK-8) and Transwell, respectively, and cell apoptosis and cycle were analyzed via fluorescent staining and flow cytometry, respectively. The regulation between gga-miR-29b-3p and its potential target genes was verified by dual luciferase results and loss-of-function assays. The effect of target genes was verified by examining the degree of RNA interference on MSB1 cells.Results: Analysis revealed that gga-miR-29b-3p impaired the proliferation of the MSB1 MD tumor cell line, induced apoptosis without obvious effects on the cell cycle, and suppressed the expression of the invasion-associated MMP2 and MMP9 genes. It was concluded that DNMT3B is the direct target of gga-miR-29b-3p. As expected, the effects of DNMT3B knockdown with small interfering RNA (siRNA) on MSB1 cell proliferation, apoptosis, and cycle were associated with gga-miR-29b-3p overexpression.Moreover, BCL2 and BCL2L1 were downregulated and TNFSF10 was upregulated in both the gga-miR-29b-3p overexpression and DNMT3B knockdown groups. The expression levels of invasion-related genes were decreased post-DNMT3B knockdown. In both the gga-miR-29b-3p overexpression and DNMT3B knockdown conditions, a decrease in MEQ oncogene expression in MD virus was observed.Conclusions: Overall, gga-miR-29b-3p was demonstrated to have a suppressive effect in MD lymphoma progression via the targeting of the DNMT3B gene. Gga-miR-29b-3p overexpression and DNMT3B knockdown inhibited MSB1 cell proliferation through suppressing the pro-apoptotic gene expression and elevating the anti-apoptotic gene expression in the apoptosis pathway. Our study provides a theoretical basis for targeted treatment of MD.

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EFLDO sensitizes liver cancer cells to TNFSF10‑induced apoptosis in a p53‑dependent manner

Cited by 9 publications

References 28 publications

An Inflammatory Response-Related Gene Signature Reveals Distinct Survival Outcome and Tumor Microenvironment Characterization in Pancreatic Cancer

An Inflammatory Response-Related Gene Signature Reveals Distinct Survival Outcome and Tumor Microenvironment Characterization in Pancreatic Cancer

MiR-581/SMAD7 Axis Contributes to Colorectal Cancer Metastasis: A Bioinformatic and Experimental Validation-Based Study

Role of gga-miR-29b-3p in suppressing the proliferation, invasion and migration of MSB1 Marek’s disease tumor cells by the targeting of the DNMT3B gene

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