CD146 mediates an E-cadherin-to-N-cadherin switch during TGF-β signaling-induced epithelial-mesenchymal transition

Ma, Yayun; Zhang, Haofeng; Xiong, Chaoliang; Zheng, Li; Xu, Qingji; Feng, Jing; Zhang, Jun; Wang, Zhaoqing; Yan, Xiyun

doi:10.1016/j.canlet.2018.05.016

Cited by 43 publications

(46 citation statements)

References 57 publications

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“…49,50 In the course of EMT, the expression levels of E-cadherin decreases, whereas the expression level of N-cadherin increases. [51][52][53] High β-catenin levels promote the expression of genes that facilitate EMT. 54 High vimentin is a biomarker in the mesenchymal state of cancer cells, mediating cytoskeletal organization, and focal adhesion maturation.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3^Tyr705 phosphorylation

Sun

Zeng

et al. 2020

Cancer Medicine

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Section: Discussionmentioning

confidence: 99%

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3^Tyr705 phosphorylation

Sun

Zeng

et al. 2020

Cancer Medicine

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“…JAK/STAT3 signaling also can be induced by oncoproteins, including RPL34 [125], HOXB8 [126], CD146 [127], and Akirin2 [128]. This recently recognized regulation of new oncogenes involved in activating JAK/STAT3/VEGFA, NF-κB, and ERK signaling might provide crucial targets to block the cancer progression.…”

Section: Other Proteins As Orchestratorsmentioning

confidence: 99%

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

Jin

2020

Cells

275

183

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The JAK/STAT3 signaling pathway plays an essential role in various types of cancers. Activation of this pathway leads to increased tumorigenic and metastatic ability, the transition of cancer stem cells (CSCs), and chemoresistance in cancer via enhancing the epithelial–mesenchymal transition (EMT). EMT acts as a critical regulator in the progression of cancer and is involved in regulating invasion, spread, and survival. Furthermore, accumulating evidence indicates the failure of conventional therapies due to the acquisition of CSC properties. In this review, we summarize the effects of JAK/STAT3 activation on EMT and the generation of CSCs. Moreover, we discuss cutting-edge data on the link between EMT and CSCs in the tumor microenvironment that involves a previously unknown function of miRNAs, and also discuss new regulators of the JAK/STAT3 signaling pathway.

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“…Global morbidity of hepatobiliary malignancies, mainly hepatocellular carcinoma (HCC) and cholangiocarcinoma, has recently increased [ 1 ]. HCC has the third highest mortality rate out of all major malignant carcinomas worldwide [ 2 ]. Surgical resection, percutaneous ablation and liver transplantation are the standard treatments for HCC, however these are only applicable to a small proportion of patients with early disease [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-302a/d inhibits the self-renewal capability and cell cycle entry of liver cancer stem cells by targeting the E2F7/AKT axis

et al. 2018

J Exp Clin Cancer Res

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BackgroundThere is increasing evidence that liver cancer stem cells (LCSCs) contribute to hepatocellular carcinoma (HCC) initiation and progression. MicroRNA (miRNA) plays a significant functional role by directly regulating respective targets in LCSCs-triggered HCC, however, little is known about the function of the miRNA-302 family in LCSCs.MethodsMiRNAs microarray was used to detect the miRNAs involved in LCSCs maintenance and differentiation. Biological roles and the molecular mechanism of miRNA-302a/d and its target gene E2F7 were detected in HCC in vitro. The expression and correlation of miRNA-302a/d and E2F7 in HCC patients was evaluated by quantitative PCR and Kaplan–Meier survival analysis.ResultsWe found that the miRNA-302 family was downregulated during the spheroid formation of HCC cells and patients with lower miRNA-302a/d expression had shorter overall survival (OS) and progression-free survival (PFS). Moreover, E2F7 was confirmed to be directly targeted and inhibited by miRNA-302a/d. Furthermore, concomitant low expression of miRNA-302a/d and high expression of E2F7 correlated with a shorter median OS and PFS in HCC patients. Cellular functional analysis demonstrated that miRNA-302a/d negatively regulates self-renewal capability and cell cycle entry of liver cancer stem cells via suppression of its target gene E2F7 and its downstream AKT/β-catenin/CCND1 signaling pathway.ConclusionsOur data provide the first evidence that E2F7 is a direct target of miRNA-302a/d and miRNA-302a/d inhibits the stemness of LCSCs and proliferation of HCC cells by targeting the E2F7/AKT/β-catenin/CCND1 signaling pathway.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0927-8) contains supplementary material, which is available to authorized users.

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CD146 mediates an E-cadherin-to-N-cadherin switch during TGF-β signaling-induced epithelial-mesenchymal transition

Cited by 43 publications

References 57 publications

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3^Tyr705 phosphorylation

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3^Tyr705 phosphorylation

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

MicroRNA-302a/d inhibits the self-renewal capability and cell cycle entry of liver cancer stem cells by targeting the E2F7/AKT axis

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CD146 mediates an E-cadherin-to-N-cadherin switch during TGF-β signaling-induced epithelial-mesenchymal transition

Cited by 43 publications

References 57 publications

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3Tyr705 phosphorylation

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3Tyr705 phosphorylation

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

MicroRNA-302a/d inhibits the self-renewal capability and cell cycle entry of liver cancer stem cells by targeting the E2F7/AKT axis

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Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3^Tyr705 phosphorylation

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3^Tyr705 phosphorylation