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

Sun, Hongzan; Zhang, Zhiqiang; Zhang, Taotao; Geng, Hao; Xie, Dongdong; Wang, Yi; Ding, Demao; Zhang, Tao; Yu, Dexin

doi:10.2147/ott.s226580

Cited by 10 publications

(12 citation statements)

References 40 publications

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“…RES can promote the expression of E-cadherin and ZO-1, and reduce the expression of N-cadherin and vimentin through STAT3/Twist signaling pathway. These findings provide new ideas for clinical prevention and intervention of bladder cancer metastasis (50).…”

Section: Genitourinary Malignancymentioning

confidence: 75%

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

et al. 2021

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Epithelial-to-mesenchymal transition (EMT), a complicated program through which polarized epithelial cells acquire motile mesothelial traits, is regulated by tumor microenvironment. EMT is involved in tumor progression, invasion and metastasis via reconstructing the cytoskeleton and degrading the tumor basement membrane. Accumulating evidence shows that resveratrol, as a non-flavonoid polyphenol, can reverse EMT and inhibit invasion and migration of human tumors via diverse mechanisms and signaling pathways. In the present review, we will summarize the detailed mechanisms and pathways by which resveratrol and its analogs (e.g. Triacetyl resveratrol, 3,5,4’-Trimethoxystilbene) might regulate the EMT process in cancer cells to better understand their potential as novel anti-tumor agents. Resveratrol can also reverse chemoresistance via EMT inhibition and improvement of the antiproliferative effects of conventional treatments. Therefore, resveratrol and its analogs have the potential to become novel adjunctive agents to inhibit cancer metastasis, which might be partly related to their blocking of the EMT process.

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Section: Genitourinary Malignancymentioning

confidence: 75%

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

et al. 2021

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“…Several natural products have been identified to attenuate EMT induced by benzidine. Resveratrol decreased smoke induced EMT in bladder cancer via STAT3/Twist1 inhibition [ 96 ]. Curcumin inhibited smoke-induced EMT as shown by an increase in the epithelial marker E-cadherin and zona occludens-1 (ZO-1) and a decrease in mesenchymal markers vimentin and N-cadherin in bladder cancer [ 97 , 98 , 99 ].…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms of Epithelial to Mesenchymal Transition Regulated by ERK5 Signaling

et al. 2021

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Extracellular signal-regulated kinase (ERK5) is an essential regulator of cancer progression, tumor relapse, and poor patient survival. Epithelial to mesenchymal transition (EMT) is a complex oncogenic process, which drives cell invasion, stemness, and metastases. Activators of ERK5, including mitogen-activated protein kinase 5 (MEK5), tumor necrosis factor α (TNF-α), and transforming growth factor-β (TGF-β), are known to induce EMT and metastases in breast, lung, colorectal, and other cancers. Several downstream targets of the ERK5 pathway, such as myocyte-specific enhancer factor 2c (MEF2C), activator protein-1 (AP-1), focal adhesion kinase (FAK), and c-Myc, play a critical role in the regulation of EMT transcription factors SNAIL, SLUG, and β-catenin. Moreover, ERK5 activation increases the release of extracellular matrix metalloproteinases (MMPs), facilitating breakdown of the extracellular matrix (ECM) and local tumor invasion. Targeting the ERK5 signaling pathway using small molecule inhibitors, microRNAs, and knockdown approaches decreases EMT, cell invasion, and metastases via several mechanisms. The focus of the current review is to highlight the mechanisms which are known to mediate cancer EMT via ERK5 signaling. Several therapeutic approaches that can be undertaken to target the ERK5 pathway and inhibit or reverse EMT and metastases are discussed.

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“…Increasing evidence demonstrates that the STAT3 pathway is capable of the induction of EMT in cancer cells, and in this way, a number of upstream mediators, such as miR-449b-3p and SIX4, act as inducers of STAT3/EMT [118,119]. The anti-tumor compounds inhibit EMT via STAT3 downregulation [120]. These studies exhibit the critical role of STAT3 in the regulation of EMT in cancer cells.…”

Section: Microrna-mediated Regulation Of Stat3mentioning

confidence: 99%

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

Ashrafizadeh

Zarrabi

Orouei

et al. 2020

Biology

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Molecular signaling pathways play a significant role in the regulation of biological mechanisms, and their abnormal expression can provide the conditions for cancer development. The signal transducer and activator of transcription 3 (STAT3) is a key member of the STAT proteins and its oncogene role in cancer has been shown. STAT3 is able to promote the proliferation and invasion of cancer cells and induces chemoresistance. Different downstream targets of STAT3 have been identified in cancer and it has also been shown that microRNA (miR), long non-coding RNA (lncRNA) and other molecular pathways are able to function as upstream mediators of STAT3 in cancer. In the present review, we focus on the role and regulation of STAT3 in gastric cancer (GC). miRs and lncRNAs are considered as potential upstream mediators of STAT3 and they are able to affect STAT3 expression in exerting their oncogene or onco-suppressor role in GC cells. Anti-tumor compounds suppress the STAT3 signaling pathway to restrict the proliferation and malignant behavior of GC cells. Other molecular pathways, such as sirtuin, stathmin and so on, can act as upstream mediators of STAT3 in GC. Notably, the components of the tumor microenvironment that are capable of targeting STAT3 in GC, such as fibroblasts and macrophages, are discussed in this review. Finally, we demonstrate that STAT3 can target oncogene factors to enhance the proliferation and metastasis of GC cells.

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

Cited by 10 publications

References 40 publications

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

Molecular Mechanisms of Epithelial to Mesenchymal Transition Regulated by ERK5 Signaling

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

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