Angiotensin Inhibition, TGF-β and EMT in Cancer

Pallasch, Fabian Bernhard; Schumacher, Udo

doi:10.3390/cancers12102785

Cited by 32 publications

(24 citation statements)

References 149 publications

(211 reference statements)

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“…As a multifunctional cytokine, TGF-β participates in numerous cell biological processes and acts on tumour cells by autocrine and paracrine. TGF-β family is closely related to EMT [ 26 ]. In tumour progression, TGF-β can activate a series of signaling pathways, including Notch [ 27 ], Wnt [ 28 ], and Smad [ 29 ] signaling pathways, and the cross-talk of these signaling pathways play a synergistic role to start the EMT process.…”

Section: Discussionmentioning

confidence: 99%

An epithelial–mesenchymal transition-related long noncoding RNA signature correlates with the prognosis and progression in patients with bladder cancer

Tong

Gao

et al. 2021

Bioscience Reports

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Bladder cancer is a common malignant tumour worldwide. Epithelial–mesenchymal transition (EMT)-related biomarkers can be used for early diagnosis and prognosis of cancer patients. To explore, accurate prediction models are essential to the diagnosis and treatment for bladder cancer. In the present study, an EMT-related long noncoding RNA (lncRNA) model was developed to predict the prognosis of patients with bladder cancer. Firstly, the EMT-related lncRNAs were identified by Pearson correlation analysis, and a prognostic EMT-related lncRNA signature was constructed through univariate and multivariate Cox regression analyses. Then, the diagnostic efficacy and the clinically predictive capacity of the signature were assessed. Finally, Gene set enrichment analysis (GSEA) and functional enrichment analysis were carried out with bioinformatics. An EMT-related lncRNA signature consisting of TTC28-AS1, LINC02446, AL662844.4, AC105942.1, AL049840.3, SNHG26, USP30-AS1, PSMB8-AS1, AL031775.1, AC073534.1, U62317.2, C5orf56, AJ271736.1, and AL139385.1 was constructed. The diagnostic efficacy of the signature was evaluated by the time-dependent receiver-operating characteristic (ROC) curves, in which all the values of the area under the ROC (AUC) were more than 0.73. A nomogram established by integrating clinical variables and the risk score confirmed that the signature had a good clinically predict capacity. GSEA analysis revealed that some cancer-related and EMT-related pathways were enriched in high-risk groups, while immune-related pathways were enriched in low-risk groups. Functional enrichment analysis showed that EMT was associated with abundant GO terms or signaling pathways. In short, our research showed that the 14 EMT-related lncRNA signature may predict the prognosis and progression of patients with bladder cancer.

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Section: Discussionmentioning

confidence: 99%

An epithelial–mesenchymal transition-related long noncoding RNA signature correlates with the prognosis and progression in patients with bladder cancer

Tong

Gao

et al. 2021

Bioscience Reports

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“…In addition, evidence has demonstrated that various signaling pathway/proteins are involved in the EMT progression of numerous cancers. Pallasch and Schumacher revealed that TGF-β, a known driver of malignancy is also an inducer of EMT in various cancers ( 43 ). It is reported that diphenyl urea derivative could serve as an inhibitor on human lung cancer cell migration by disrupting EMT via Wnt/β-catenin and PI3K/Akt signaling ( 44 ).…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic acid induces apoptosis, inhibits metastasis and improves antitumor immunity in breast cancer via the NF‑κB signaling pathway

et al. 2020

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Breast cancer which is the most common type of diagnosed cancer among women worldwide possesses metastatic potential, multi-drug resistance, and high mortality. The NF-κB signaling pathway has been revealed to be abnormally activated in breast cancer cells and closely associated with high metastasis and poor prognosis. In the present study, it was reported that chlorogenic acid (CGA), a potent NF-κB inhibitor derived from coffee, exerted antitumor activity in breast cancer. MTT and colony formation assays were conducted and it was revealed that CGA inhibited viability and proliferation in breast cancer cells. Additionally, CGA significantly induced apoptosis and suppressed migration and invasion in breast cancer cells. Notably, immunofluorescence analysis confirmed that CGA could efficiently suppress nuclear transcription of NF-κB p65. In addition, results of western blotting demonstrated that CGA markedly impaired the NF-κB and EMT signaling pathways. The antitumor effect of CGA was evaluated in a subcutaneous tumor mouse model of 4T1 cells, and the results revealed that CGA markedly retarded tumor growth and prolonged the survival rate of tumor-bearing mice. Notably, CGA inhibited pulmonary metastasis of 4T1 cells by enhancing the proportion of CD4 + and CD8 + T cells in spleens of mice, which indicated an improvement of antitumor immunity. In conclusion, the present present study demonstrated that CGA improved antitumor immunity, exerting antitumor and anti-metastatic effects by impairing the NF-κB/EMT signaling pathway, suggesting that CGA may serve as a potential candidate for therapy of breast cancer.

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“…Adjacent cells may communicate with each other through different mechanisms. Secretion of a specific chemokine, such as TGF-β, is one of the most investigated mechanisms in tumour–stroma interaction [ 67 , 68 , 69 ] ( Table 1 ). Active molecules may be released by different cell types, and they may target several other cells.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Mechanisms beyond Tumour–Stroma Crosstalk

Gagliano

Brancolini

2021

Cancers

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Despite cancer having been usually considered the result of genetic mutations, it is now well established that epigenetic dysregulations play pivotal roles in cancer onset and progression. Hence, inactivation of tumour suppressor genes can be gained not only by genetic mutations, but also by epigenetic mechanisms such as DNA methylation and histone modifications. To occur, epigenetic events need to be triggered by genetic alterations of the epigenetic regulators, or they can be mediated by intracellular and extracellular stimuli. In this last setting, the tumour microenvironment (TME) plays a fundamental role. Therefore, to decipher how epigenetic changes are associated with TME is a challenge still open. The complex signalling between tumour cells and stroma is currently under intensive investigation, and most of the molecules and pathways involved still need to be identified. Neoplastic initiation and development are likely to involve a back-and-forth crosstalk among cancer and stroma cells. An increasing number of studies have highlighted that the cancer epigenome can be influenced by tumour microenvironment and vice versa. Here, we discuss about the recent literature on tumour–stroma interactions that focus on epigenetic mechanisms and the reciprocal regulation between cancer and TME cells.

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Angiotensin Inhibition, TGF-β and EMT in Cancer

Cited by 32 publications

References 149 publications

An epithelial–mesenchymal transition-related long noncoding RNA signature correlates with the prognosis and progression in patients with bladder cancer

An epithelial–mesenchymal transition-related long noncoding RNA signature correlates with the prognosis and progression in patients with bladder cancer

Chlorogenic acid induces apoptosis, inhibits metastasis and improves antitumor immunity in breast cancer via the NF‑κB signaling pathway

Epigenetic Mechanisms beyond Tumour–Stroma Crosstalk

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