Twist1 is highly expressed in cancer-associated fibroblasts of esophageal squamous cell carcinoma with a prognostic significance

Yeo, So-Young; Ha, Sang-Yun; Lee, Keun-Woo; Cui, Yan; Yang, Zheng; Xuan, Yanhua; Kim, Seok-Hyung

doi:10.18632/oncotarget.17941

Cited by 25 publications

(25 citation statements)

References 14 publications

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“…The correlation between STAT3 and TWIST was analyzed by biluciferase, and the results showed that STAT3 could improve the transcriptional activity of TWIST1 and promote EMT, thus enhancing the invasion and metastatic capacity of liver cancer cells. 34 TWIST1 expression was significantly reduced after a STAT3 inhibitor was used. TWIST1 is considered to be an important factor in the regulation of E-Cadherin, which plays a role mainly through the STAT3/TWIST1 signaling pathway axis.…”

Section: Dovepressmentioning

confidence: 98%

<p>Resveratrol Reverses Cigarette Smoke-Induced Urocystic Epithelial–Mesenchymal Transition via Suppression of STAT3 Phosphorylation in SV-HUC-1-Immortalized Human Urothelial Cells</p>

Sun¹,

Zhang²,

Zhang³

et al. 2019

OTT

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Purpose: Bladder cancer is a malignant tumor of the urinary tract, and cigarette smoke (CS) is closely related to tumorigenesis. Resveratrol, a plant-derived bioactive nutrient, possesses multiple anticancer effects. However, the mechanism of CS-induced tumorigenesis is still not clear. The role of resveratrol in CS-meditated bladder cancer development has not been reported. Methods: MTT assay showed the toxicity of cigarette smoke extract (CSE) on the cell viability of SV-HUC-1 cells. Western blotting detected the expression levels of related proteins. Transwell migration or invasion assay evaluated the capacity of cell migration or invasion after treatment. Wound-healing assay revealed the effect of cell migratory capacity. The cell cycle was detected by flow cytometry. Results: Our study demonstrated that CSE-triggered epithelial-mesenchymal transition (EMT) in SV-HUC-1-immortalized human urothelial cells via the STAT3/TWIST1 pathway. Furthermore, the results showed resveratrol effectively inhibited STAT3 phosphorylation, thus reversed EMT triggered by CSE. Meanwhile, the cell proliferation was also suppressed. Conclusion: In conclusion, inhibition of the STAT3 in CSE-induced EMT on bladder cancer may be a promising cancer treatment target for suppression by resveratrol.

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Section: Dovepressmentioning

confidence: 98%

<p>Resveratrol Reverses Cigarette Smoke-Induced Urocystic Epithelial–Mesenchymal Transition via Suppression of STAT3 Phosphorylation in SV-HUC-1-Immortalized Human Urothelial Cells</p>

Sun¹,

Zhang²,

Zhang³

et al. 2019

OTT

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“…Has been shown to be an important driver of metastasis. 28,[70][71][72] No PDPN Often overexpressed in certain CAF subtypes. Unspecific for fibroblasts and expressed by tumor cells and macrophages.…”

Section: Pdgfrα/βmentioning

confidence: 99%

“…PDGFRα is much more widely expressed over the larger fibroblast population than more specific markers such as αSMA. 29,70,73,74 Yes VIM Traditional marker for fibroblast identification. Not CAF-specific and widely expressed by all fibroblasts.…”

Section: Fibroblast Markersmentioning

confidence: 99%

In search of definitions: Cancer‐associated fibroblasts and their markers

Nurmik

Ullmann

Rodriguez

et al. 2019

Intl Journal of Cancer

426

382

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The tumor microenvironment has been identified as one of the driving factors of tumor progression and invasion. Inside this microenvironment, cancer‐associated fibroblasts (CAFs), a type of perpetually activated fibroblasts, have been implicated to have a strong tumor‐modulating effect and play a key role in areas such as drug resistance. Identification of CAFs has typically been carried based on the expression of various “CAF markers”, such as fibroblast activation protein alpha (FAP) and alpha smooth muscle actin (αSMA), which separates them from the larger pool of fibroblasts present in the body. However, as outlined in this Review, the expression of various commonly used fibroblast markers is extremely heterogeneous and varies strongly between different CAF subpopulations. As such, novel selection methods based on cellular function, as well as further characterizing research, are vital for the standardization of CAF identification in order to improve the cross‐applicability of different research studies in the field. The aim of this review is to give a thorough overview of the commonly used fibroblast markers in the field and their various strengths and, more importantly, their weaknesses, as well as to highlight potential future avenues for CAF identification and targeting.

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“…Twist1/G3BP2 signaling responds to biomechanical signaling from the microenvironment with invasion and tumor spread and drives cell transition and metastasis [144]. The pro-inflammatory mediator, interleukin 6 (IL-6), enhances Twist1 in fibroblasts and STAT3 phosphorylation with consequent cancer-associated fribroblast transdifferentiation [145,146]. Furthermore, Twist1 upregulates the nuclear transcriptor protein paired related homeobox 1 (Prrx1) which increases the glycoprotein Tenascin-C (TNC) with consequent positive feedback loop (PFL) by enhancing Twist1 again.…”

Section: Fibrosis and Its Remodeling Resulting Into The Precancerous mentioning

confidence: 99%

“…Furthermore, Twist1 upregulates the nuclear transcriptor protein paired related homeobox 1 (Prrx1) which increases the glycoprotein Tenascin-C (TNC) with consequent positive feedback loop (PFL) by enhancing Twist1 again. The continous Twist1-Prrx1-TNC PFL interaction results in fibrosis in vivo in fibrotic disease and cancer-assosicated stroma and this positive feedback loop can become irreversibly activated [146,147].…”

Section: Fibrosis and Its Remodeling Resulting Into The Precancerous mentioning

confidence: 99%

Transition from normal to cancerous cell by precancerous niche (PCN) induced chronic cell-matrix stress

Brücher

Jamall

2019

4open

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The attempt to restore homeostasis, once disrupted, such that complex signaling, crosstalk between ubiquitous proteins, and a diverse range of pathways gone awry is near impossible, especially in the presence of an ongoing pathogenic stimuli with incessant inflammation. This persistent inflammation, when unresolved, induces fibrosis with consequent remodeling of the extracellular matrix (ECM) which leads to the formation of the precancerous niche (PCN), the tipping point in the transition of normal to cancerous cells. Thus, the sustained disruption of homeostasis when confronted with limited adaptation capabilities either of cells or of the surrounding matrix and faced with chronic stress in the tissue microenvironment results in an escape strategy which, if unsuccessful, causes cells, tissue, or the organism to become unable to recover over the long term. All conditions necessary for cell–cell transition such as deregulation of cell–cell complexes, decrease in the stability of adherens junctions, together with the apical-basal polarity, and the loss of the cytoskeletal architecture occurs as a cascade of events inducing inappropriate and diverse signaling pathways and crosstalk. In biology, the transition of one cell type to another and the transition from one cell function to another is incompletely understood mechanistically, but within the context of embryogenesis and morphogenesis is acknowledged as a physiologically routine event. The constant stress that can result in the development of the PCN leads to a chronic stress escape strategy (CSES) which, if unsuccessful, eventually triggers a normal cell- to-cancer cell- transition (NCCCT).

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Twist1 is highly expressed in cancer-associated fibroblasts of esophageal squamous cell carcinoma with a prognostic significance

Cited by 25 publications

References 14 publications

<p>Resveratrol Reverses Cigarette Smoke-Induced Urocystic Epithelial–Mesenchymal Transition via Suppression of STAT3 Phosphorylation in SV-HUC-1-Immortalized Human Urothelial Cells</p>

<p>Resveratrol Reverses Cigarette Smoke-Induced Urocystic Epithelial–Mesenchymal Transition via Suppression of STAT3 Phosphorylation in SV-HUC-1-Immortalized Human Urothelial Cells</p>

In search of definitions: Cancer‐associated fibroblasts and their markers

Transition from normal to cancerous cell by precancerous niche (PCN) induced chronic cell-matrix stress

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