Extracellular vesicles released by mesenchymal-like prostate carcinoma cells modulate EMT state of recipient epithelial-like carcinoma cells through regulation of AR signaling

El-Sayed, Ihsan Y.; Daher, Ahmad; Destouches, Damien; Firlej, Virginie; Kostallari, Enis; Maillé, Pascale; Huet, Eric; Haidar-Ahmad, Nathaline; Jenster, Guido; Taille, Alexandre de la; Merhi, Raghida Abou; Terry, Stéphane; Vacherot, Francis

doi:10.1016/j.canlet.2017.09.010

Cited by 29 publications

(33 citation statements)

References 42 publications

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“…The interplays between AR and exosome pathways has been also highlighted in a recent experiment that used a variant of 22Rv1cells ( 140 ). Obtained by stable expression of the CRIPTO protein (an epidermal growth factor-related protein), this variant named Mes-PCa cells displays mesenchymal features that are accompanied by an increased released of EVs when comparing to parental cells.…”

Section: Biological Functions Of Exosomes In Prostate Cancermentioning

confidence: 90%

Extracellular Vesicles in Prostate Cancer Carcinogenesis, Diagnosis, and Management

Vlaeminck-Guillem

2018

Front. Oncol.

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Extracellular vesicles (EVs), especially exosomes, are now well recognized as major ways by which cancer cells interact with each other and stromal cells. The meaningful messages transmitted by the EVs are carried by all components of the EVs, i.e., the membrane lipids and the cargo (DNAs, RNAs, microRNAs, long non-coding RNAs, proteins). They are clearly part of the armed arsenal by which cancer cells obtain and share more and more advantages to grow and conquer new spaces. Identification of these messages offers a significant opportunity to better understand how a cancer occurs and then develops both locally and distantly. But it also provides a powerful means by which cancer progression can be detected and monitored. In the last few years, significant research efforts have been made to precisely identify how the EV trafficking is modified in cancer cells as compared to normal cells and how this trafficking is altered during cancer progression. Prostate cancer has not escaped this trend. The aim of this review is to describe the results obtained when assessing the meaningful content of prostate cancer- and stromal-derived EVs in terms of a better comprehension of the cellular and molecular mechanisms underlying prostate cancer occurrence and development. This review also deals with the use of EVs as powerful tools to diagnose non-indolent prostate cancer as early as possible and to accurately define, in a personalized approach, its present and potential aggressiveness, its response to treatment (androgen deprivation, chemotherapy, radiation, surgery), and the overall patients’ prognosis.

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Section: Biological Functions Of Exosomes In Prostate Cancermentioning

confidence: 90%

Extracellular Vesicles in Prostate Cancer Carcinogenesis, Diagnosis, and Management

Vlaeminck-Guillem

2018

Front. Oncol.

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“…In addition, the results demonstrated that FOXK2 overexpression reduced cell invasion, growth and proliferation. EMT is a critical step in cancer metastasis ( 27 , 28 ); during EMT, epithelial cells change phenotype and obtain the characteristics of mesenchymal cells, gaining the ability to migrate and contribute to tumor metastasis ( 29 – 31 ). EMT is accompanied by an alteration in the expression of several proteins, including N-cadherin, E-cadherin, TWIST, SNAIL and β-catenin ( 16 ).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of FOXK2 is associated with poor prognosis in patients with gastric cancer

et al. 2018

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Forkhead box (FOX)K2 (FOXK2) is a member of the FOX transcription factor family. It has been suggested previously that FOXK2 is required to suppress tumor growth; however, the exact role of FOXK2 in gastric cancer remains to be elucidated. In the present study, the association between FOXK2 expression and the clinicopathological characteristics of patients with gastric cancer was investigated. The prognostic value of FOXK2 expression and the significance of clinicopathological parameters in the overall survival (OS) and progression-free survival of patients were also determined by survival analysis. To investigate the functional roles of FOXK2, it was downregulated in BGC-823 cells using small interfering (si)RNA, and upregulated using a FOXK2 plasmid. Colony formation, Cell Counting Kit-8 and cell proliferation analyses were conducted to examine the proliferation of gastric cancer cells. Transwell and wound-healing assays were performed to investigate the effect of FOXK2 expression on gastric cancer cell migration and invasion. The clinical data demonstrated that FOXK2 expression was reduced in high-grade gastric cancer tissues, and a low level of FOXK2 expression indicated a poor prognosis. The data obtained from the Human Protein Atlas revealed that patients with gastric cancer and a high level of FOXK2 expression had a longer OS time. The results of colony formation assays, Transwell and wound healing assays demonstrated that FOXK2 repressed the proliferation, invasion and migration of gastric cancer cells, respectively. The findings indicated that FOXK2 may serve as a promising therapeutic target in gastric cancer. Taken together, the findings of the present study demonstrated that FOXK2 functions as a tumor suppressor in gastric cancer; the loss of FOXK2 may induce the growth and invasion of gastric cancer cells.

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“…Moreover, we found that FOXK1 also reduces cell migration and invasion through the regulation of EMT. EMT is a critical step in cancer metastasis, 27,28 epithelial cells change phenotype and obtain the characteristics of mesenchymal cells, gaining the ability to migrate and contribute to tumor metastasis. 29 During EMT process, the expression of several proteins is alteration, such as epithelial marker E-cadherin, mesenchymal markers N-cadherin and vimentin, EMT-associated transcription factors TWIST, Snail and Slug.…”

Section: Discussionmentioning

confidence: 99%

<p>FOXK1, Regulated by miR-365-3p, Promotes Cell Growth and EMT Indicates Unfavorable Prognosis in Breast Cancer</p>

Gao¹,

Tian²

2020

OTT

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Background: Forkhead box K1 (FOXK1) is members of the FOX transcription factor family. Previous work has found out that FOXK1 promotes cell proliferation, migration and invasion in several cancers, such as gastric cancer, glioma cancer and lung cancer; however, the exact role of FOXK1 in breast cancer is still poorly known. Methods: Here, the association between FOXK1 expression and the clinicopathological characteristics of patients with breast cancer was identified. To further decipher the functional roles of FOXK1, it was overexpressed or knocked down in MCF-7, MDA-MB-231 and MCF-10A cells. Cell Counting Kit-8, colony formation and cell cycle assays were performed to examine the proliferation of breast cancer cells. Moreover, wound-healing and Transwell invasion analyses were carried out to explore the effect of FOXK1 on breast cancer cell migration and invasion. Results: Our findings discovered that FOXK1 promotes cell proliferation, migration and invasion in breast cancer. In addition, consistent with the previous report, FOXK1 also facilitates EMT in breast cancer. TargetScan was used to predict upstream of FOXK1, indicating that miR-365-3p could regulate FOXK1 expression in breast cancer. Conclusion: The findings of the present study demonstrated that miR-365-3p-FOXK1 axis plays a key role in breast cancer.

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Extracellular vesicles released by mesenchymal-like prostate carcinoma cells modulate EMT state of recipient epithelial-like carcinoma cells through regulation of AR signaling

Cited by 29 publications

References 42 publications

Extracellular Vesicles in Prostate Cancer Carcinogenesis, Diagnosis, and Management

Extracellular Vesicles in Prostate Cancer Carcinogenesis, Diagnosis, and Management

Downregulation of FOXK2 is associated with poor prognosis in patients with gastric cancer

<p>FOXK1, Regulated by miR-365-3p, Promotes Cell Growth and EMT Indicates Unfavorable Prognosis in Breast Cancer</p>

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