Impact of TGF-β1 expression and -509C&gt;T polymorphism in the TGF-β1 gene on the progression and survival of gastric cancer

Ananiev, Julian; Manolova, Irena; Aleksandrova, Elina; Gulubova, Maya

doi:10.5114/pjp.2017.71530

Cited by 3 publications

(2 citation statements)

References 8 publications

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“…It is well-known that there is TGF-β1 expression with high level in cancer cells. Ananiev et al reported that the expression of TGF-β1 in the gastric cancer patients was associated with shorter survival time and rapid progression (29). Generally, TGF-β1 can induce EMT in various cancer cells, such as breast cancer cells, hepatocellular carcinoma and neuroblastoma cells (30)(31)(32).…”

Section: Discussionmentioning

confidence: 99%

EDIL3 regulates gastric cancer cell migration, invasion and epithelial-mesenchymal transition via TGF-β1/XIST/miR-137 feedback loop

Zhang¹,

Peng²,

Wang³

et al. 2020

Transl Cancer Res TCR

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Background: Human gastric cancer is a serious disease with high mortality rate all over the world. The one of difficulties in effective therapy of gastric cancer is metastasis. It has been reported that lncRNAs and miRNAs are involved in cancer metastasis. So, exploration of new molecular mechanism underlying gastric cancer metastasis involving in network of lncRNAs/miRNAs/effector proteins is important and meaningful for guiding the treatment of gastric cancer.Methods: MTT assay, flow cytometric analysis and colony formation assay were performed to evaluate AGS or MKN-45 cell proliferation, cycle distribution and colony formation, and RT-qPCR was used to examine the expressive abundances of EDIL3, XIST and miR-137. EDIL3 and epithelial-mesenchymal transition (EMT) related proteins were detected by western blot and migration and invasion were measured by transwell analysis. Meanwhile, dual-luciferase reporter assay was used to confirm XIST binding to miR-137, and miR-137 binding to EDIL3. AGS cells were used to establish the xenograft tumor model to verify the role of EDIL3 in tumorigenesis in nude mice.Results: Expression levels of EDIL3 were increased in gastric cancer tissues and cell lines. Downregulation of EDIL3 or XIST and overexpression of miR-137 inhibited proliferation, migration, invasion and EMT in AGS and MKN-45 cells. XIST could specifically bind to miR-137, and EDIL3 was a target gene of miR-137. Moreover, TGF-β1 stimulated XIST expression, inhibited miR-137 expression and induced migration, invasion and EMT. We also found that overexpression of EDIL3 elevated levels of TGF-β1 and induced migration, invasion and EMT, which were reversed by TGF-β1 inhibition. EDIL3 knockdown suppressed migration, invasion and EMT, which were reversed by XIST. Overexpression of miR-137 inhibited proliferation, migration, invasion and EMT, which were reversed by EDIL3 overexpression.Conclusions: EDIL3 regulates gastric cancer cell migration, invasion and EMT, which is involved in the regulation of TGF-β1/XIST/miR-137 feedback loop, and EDIL3 knockdown inhibits tumor growth in nude mice. These findings indicate that the EDIL3 mediated molecular feedback loop may be developed as drug targets for the gastric carcinoma treatment.

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Section: Discussionmentioning

confidence: 99%

EDIL3 regulates gastric cancer cell migration, invasion and epithelial-mesenchymal transition via TGF-β1/XIST/miR-137 feedback loop

Zhang¹,

Peng²,

Wang³

et al. 2020

Transl Cancer Res TCR

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“…Inconsistent with these observations, our results indicated a shorter overall survival after operation for the carriers of the T/T-genotype with high-grade glial tumors compared to the carriers of at least one C-allele, although it should be noted that the survival functions did not find statistical significance. Nevertheless, the negative effect of the T-allele on overall patient survival has been reported widely in other types of cancer, such as colorectal [24], non-small-cell lung cancer [27], and gastric cancer [28].…”

Section: Discussionmentioning

confidence: 99%

Role of Elevated Serum TGF-β1 and the Common Promoter TGFB1-509C/T Polymorphism in the Development and Progression of Primary Glial Tumors and Brain Metastases

Aleksandrova,

Mindov,

Petrov

et al. 2024

Medicina

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Background and Objectives: The role of transforming growth factor-beta1 (TGF-β1) has been widely studied in the context of carcinogenesis. It has been involved in the pathogenesis of primary brain tumors or brain metastases due to its pleiotropic effects on immune regulation and tissue homeostasis. In line with recent findings, the aim of the current study was to examine the role of circulating TGF-β1 and the -509C/T functional polymorphism (rs1800469) in the TGFB1 gene promoter in the susceptibility and progression of primary brain tumors and brain metastases among patients from the Bulgarian population. Materials and Methods: Cases with a confirmed diagnosis were genotyped by the polymerase chain reaction-restriction fragment length polymorphism assay (PCR-RFLP). Serum TGF-β1 levels were determined by ELISA. Immunohistochemical evaluation of the expression of TGF-β1 and the TGF-β1 receptor-type II was conducted. Results: We observed that TGF-β1 serum levels correlate with the genotype and are sex-related. TGF-β1 serum levels were significantly elevated in patients compared to controls. Additionally, the T/T-genotype determined higher circulating levels of the cytokine. The same genotype determined the shorter median survival after surgery for the patients. The immunohistochemical analysis revealed a statistical tendency: cases expressing TGF-β1 in the cytoplasm had elevated levels of the cytokine in the serum compared to the negative cases. Conclusions: Overall, our results indicate a negative effect of the T-allele on the predisposition and prognosis of brain malignancies, and the genetically determined higher TGF-β1 serum levels might contribute to the worse prognosis and metastatic capacity of brain malignancies.

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lncRNA polymorphism affects the prognosis of gastric cancer

et al. 2022

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Background Previous studies have found that lncRNA polymorphisms are associated with the prognosis of gastric cancer (GC), but the specific roles of many lncRNA polymorphism sites in gastric cancer are still unclear. Our study aims to deeply explore the relationship between genetic polymorphism of lncRNA and the prognosis of GC. Methods The genotypes of candidate SNP locus were detected by Sequenom Mass ARRAY SNP. We deeply analyzed the association of lncRNA polymorphisms with GC prognosis by univariate and multivariate Cox regression, stratified analysis, conjoint analysis, and log-rank test. Results We found that mutations at rs2579878 and rs10036719 loci reduced the risk of poor prognosis of GC. Stratified analysis showed that rs2795025, rs10036719, and rs12516079 polymorphisms were all associated with tumor prognosis. In addition, conjoint analyses showed that the interaction between these two polymorphic sites (rs2795025 and rs12516079) could increase the risk of poor prognosis. Multivariate analysis also found that the AG/AA genotype of rs10036719 and AG genotype of rs12516079 were independent prognostic factors. Moreover, the high expression of both CCDC26 and LINC02122 were shown to be associated with the poor survival status of GC patients. Conclusions We find that the genetic polymorphism of lncRNA plays a role in the development of GC and is closely related to the survival time of patients. It could serve as a predictor of the prognosis of GC.

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Impact of TGF-β1 expression and -509C>T polymorphism in the TGF-β1 gene on the progression and survival of gastric cancer

Cited by 3 publications

References 8 publications

EDIL3 regulates gastric cancer cell migration, invasion and epithelial-mesenchymal transition via TGF-β1/XIST/miR-137 feedback loop

EDIL3 regulates gastric cancer cell migration, invasion and epithelial-mesenchymal transition via TGF-β1/XIST/miR-137 feedback loop

Role of Elevated Serum TGF-β1 and the Common Promoter TGFB1-509C/T Polymorphism in the Development and Progression of Primary Glial Tumors and Brain Metastases

lncRNA polymorphism affects the prognosis of gastric cancer

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