TGF-β1 mediates estrogen receptor-induced epithelial-to-mesenchymal transition in some tumor lines

Fan, Daiming; Qi, Pengwei; Gao, Shegan; Chen, Yawei; Cheng, Xiaolin

doi:10.1007/s13277-014-2166-8

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…EMT is involved in processes such as embryonic development, organ fibrosis, tissue damage and repair, and tumor metastasis ( Nieto et al, 2016 ; Zhang and Weinberg, 2018 ). Estrogen can induce EMT through the Notch signaling pathway ( Li et al, 2018 ), Wnt/β-catenin signaling pathway ( Zhou et al, 2012 ), and TGF-β/Smad signaling pathway ( Fan et al, 2014 ), thus promoting AM formation. The decrease in E-cadherin paralleled by the increase in vimentin and N-cadherin is an important feature of EMT and a pattern also observed in AM lesions, indicating that EMT promotes the development of AM ( Chen et al, 2010 ; An et al, 2017 ) ( Figure 3C ).…”

Section: Pathogenesis Of Ammentioning

confidence: 99%

Exosomes: potential diagnostic markers and drug carriers for adenomyosis

Cheng,

Wei,

Zhou

et al. 2023

Front. Pharmacol.

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Adenomyosis is a common benign gynecological disorder and an important factor leading to infertility in fertile women. Adenomyosis can cause deep lesions and is persistent and refractory in nature due to its tumor-like biological characteristics, such as the ability to implant, adhere, and invade. The pathogenesis of adenomyosis is currently unclear. Therefore, new therapeutic approaches are urgently required. Exosomes are nanoscale vesicles secreted by cells that carry proteins, genetic materials and other biologically active components. Exosomes play an important role in maintaining tissue homeostasis and regulating immune responses and metabolism. A growing body of work has shown that exosomes and their contents are key to the development and progression of adenomyosis. This review discusses the current research progress, future prospects and challenges in this emerging therapeutic tool by providing an overview of the changes in the adenomyosis uterine microenvironment and the biogenesis and functions of exosomes, with particular emphasis on the role of exosomes and their contents in the regulation of cell migration, proliferation, fibrosis formation, neovascularization, and inflammatory responses in adenomyosis.

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Section: Pathogenesis Of Ammentioning

confidence: 99%

Exosomes: potential diagnostic markers and drug carriers for adenomyosis

Cheng,

Wei,

Zhou

et al. 2023

Front. Pharmacol.

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Silencing of HMGA2 suppresses cellular proliferation, migration, invasion, and epithelial–mesenchymal transition in bladder cancer

Shi

et al. 2015

Tumor Biol.

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The high-mobility group protein A2 (HMGA2) is an architectural transcription factor that plays a crucial role in the development and progression of various malignant cancers. However, the function of HMGA2 in bladder cancer remains largely unknown. Therefore, we aim to investigate the effect of HMGA2 on the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of bladder cancer cells. The expression of HMGA2 in human bladder cancer cells was downregulated by small interfering RNA (siRNA). The protein levels of HMGA2 and other related proteins were detected by Western blotting. The cell proliferation and apoptosis were examined by Cell Counting Kit-8 and flow cytometry, respectively. Transwell migration and invasion assays were performed to assess the effect of HMGA2 on the migration and invasion ability of cells. In conclusion, we found that HMGA2 knockdown markedly inhibited cell proliferation; this reduced cell growth was due to the high apoptosis rate of cells, as Bcl-xl was diminished, whereas Bax was upregulated. Moreover, our results showed that silencing of HMGA2 in cancer cells greatly inhibited the cell migration and invasion, decreased the expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9), and affected the occurrence of EMT. We further found that decreased HMGA2 expression suppressed the transforming growth factor-β (TGF-β)/Smad and Wnt/β-catenin signaling pathway in bladder cancer cells. These results revealed that HMGA2 played an important role in the progression of bladder cancer and might be a novel target for therapy in human bladder cancer.

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TGF-β1 mediates estrogen receptor-induced epithelial-to-mesenchymal transition in some tumor lines

Cited by 2 publications

References 21 publications

Exosomes: potential diagnostic markers and drug carriers for adenomyosis

Exosomes: potential diagnostic markers and drug carriers for adenomyosis

Silencing of HMGA2 suppresses cellular proliferation, migration, invasion, and epithelial–mesenchymal transition in bladder cancer

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