EMT in cervical cancer: Its role in tumour progression and response to therapy

Qureshi, Rehana; Arora, Himanshu; Rizvi, Abbas

doi:10.1016/j.canlet.2014.09.021

Cited by 221 publications

(219 citation statements)

References 159 publications

(204 reference statements)

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“…[20,39] During MET, elongated spindle-shaped cells acquire an epithelial morphology, with a large nuclear-to-cytoplasmic ratio. [40][41][42][43][44] Thus, to examine whether the substrate stiffness affects MET during reprogramming, we measured morphological changes of MEFs and the expression of MET markers when cells were cultured on the various substrates. MEFs grown on the 0.1 kPa hydrogel exhibited an epithelial morphology with a high nuclear-to-cytoplasmic ratio.…”

Section: Substrate Stiffness Regulates Metmentioning

confidence: 99%

Stiffness of Hydrogels Regulates Cellular Reprogramming Efficiency Through Mesenchymal‐to‐Epithelial Transition and Stemness Markers

Choi

Park

Kim

et al. 2015

Macromolecular Bioscience

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The stiffness of hydrogels has been reported to direct cell fate. Here, we found that the stiffness of hydrogels promotes the reprogramming of mouse embryonic fibroblasts into induced pluripotent stem cells (iPSCs). We prepared cell culture substrates of various stiffnesses (0.1, 1, 4, 10, and 20 kPa) using a polyacrylamide hydrogel. We found that culture on a soft hydrogel plays an important role in inducing cellular reprogramming into iPSCs via activation of mesenchymal-to-epithelial transition and enhancement of stemness marker expression. These results suggest that physical signals at the interface between cell and substrate can be used as a potent regulator to promote cell fate changes associated with reprogramming into iPSCs, which may lead to effective and reproducible iPSC-production.

show abstract

Section: Substrate Stiffness Regulates Metmentioning

confidence: 99%

Stiffness of Hydrogels Regulates Cellular Reprogramming Efficiency Through Mesenchymal‐to‐Epithelial Transition and Stemness Markers

Choi

Park

Kim

et al. 2015

Macromolecular Bioscience

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“…EMT has been proposed to have a critical role in the initiation of metastasis progression of cancer (20,21). To gain a mechanistic illustration of the potential role of miR-1297 in modulating CC metastasis, EMT markers were assessed.…”

Section: Mir-1297 Inhibits CC Cell Migration and Invasion In Vitromentioning

confidence: 99%

MicroRNA-1297 inhibits metastasis and epithelial-mesenchymal transition by targeting AEG-1 in cervical cancer

Wang

Guo

et al. 2017

Oncology Reports

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Abstract. Accumulating evidence has demonstrated that aberrant miRNAs contribute to cervical cancer (CC) development and progression. However, the roles of various miRNAs in CC remain to be determined. In the present study, we confirmed that a decreased miR-1297 expression was present in CC tissues and cell lines. Our clinical analysis revealed that the downregulated miR-1297 expression was significantly correlated with poor prognostic features including lymph node metastasis and lymphovascular space invasion. Moreover, we confirmed that miR-1297 was a novel independent prognostic marker for predicting the 5-year survival of CC patients. The ectopic overexpression of miR-1297 inhibited cell migration, invasion and EMT progression, while downregulated miR-1297 reversed these effects. In addition, miR-1297 regulated AEG-1 by directly binding to its 3'-UTR. In clinical samples of CC, miR-1297 was inversely correlated with AEG-1, which was upregulated in CC. Alteration of AEG-1 expression at least partially abolished the migration, invasion and EMT progression effects of miR-1297 on CC cells. In conclusion, our results indicated that miR-1297 functioned as a tumor suppressor gene in regulating the EMT and metastasis of CC via targeting of AEG-1, and may represent a novel potential therapeutic target and prognostic marker for CC.

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“…1Y3 Recent investigations suggested that HPV pushes cancer progression through epithelial-mesenchymal transition (EMT) event. 4,5 The initial stage of cervical cancer is associated with morphogenetic change from epithelial cells to fibroblast-like cells, that is, EMT. As the degree of EMT is increasing, the cells gradually lose the polarization, disassemble the junctions, increase the mobility, invade the basement membrane beneath, enter the blood vessels, and disseminate into secondary organs.…”

mentioning

confidence: 99%

“…4Y6 The process is represented by the stepwise progression from cervicitis to cervical intraepithelial neoplasia and further to primary invasive carcinoma without metastasis (unmetastatic cervical squamous cell carcinoma [un-SCC]) and then to metastatic cervical squamous cell carcinoma (met-SCC). 4,5 A series of molecular events occurs in EMT program. 6,7 Downregulation of E-cadherin (E-cad) is considered as a critical point and a molecular hallmark of EMT.…”

mentioning

confidence: 99%

Y Box-Binding Protein 1 Promotes Epithelial-Mesenchymal Transition, Invasion, and Metastasis of Cervical Cancer via Enhancing the Expressions of Snail

Pang¹,

Zhang

et al. 2017

International Journal of Gynecological Cancer

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The results firstly reported that YB-1 whose mRNA expression is regulated by HPV18 E6 promotes epithelial-mesenchymal transition and progression of cervical cancer via enhancing the expressions of Snail, which indicated that YB-1/Snail/epithelial-mesenchymal transition axis could have a potential use in the diagnosis and therapy of cervical cancer metastasis as a cancer marker and molecular target.

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EMT in cervical cancer: Its role in tumour progression and response to therapy

Cited by 221 publications

References 159 publications

Stiffness of Hydrogels Regulates Cellular Reprogramming Efficiency Through Mesenchymal‐to‐Epithelial Transition and Stemness Markers

Stiffness of Hydrogels Regulates Cellular Reprogramming Efficiency Through Mesenchymal‐to‐Epithelial Transition and Stemness Markers

MicroRNA-1297 inhibits metastasis and epithelial-mesenchymal transition by targeting AEG-1 in cervical cancer

Y Box-Binding Protein 1 Promotes Epithelial-Mesenchymal Transition, Invasion, and Metastasis of Cervical Cancer via Enhancing the Expressions of Snail

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