Mesenchymal to epithelial transition in sarcomas

Yang, Jilong; Du, Xiaoling; Wang, Guowen; Sun, Yan; Chen, Kexin; Zhu, Xiong-Zeng; Lazar, Alexander J.; Hunt, Kelly K.; Pollock, Raphael E.; Zhang, Wei

doi:10.1016/j.ejca.2013.11.006

Cited by 45 publications

(61 citation statements)

References 47 publications

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“…Aberrant activation of EMT has been reported to contribute to tumour progression/metastasis. During metastasis-associated MET, the epithelial tumour cells, which have undergone EMT and are present in the blood circulation, reverse the EMT process to grow at distant sites as epithelial tumour cells (2,3). Sarcoma metastasis is not well understood (1).…”

Section: Introductionmentioning

confidence: 99%

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Galoian

Qureshi

Wideroff

et al. 2014

Molecular and Clinical Oncology

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Abstract. Disruption of cell-cell junctions and the concomitant loss of polarity, downregulation of tumor-suppressive adherens junctions and desmosomes represent hallmark phenotypes for several different cancer cells. Moreover, a variety of evidence supports the argument that these two common phenotypes of cancer cells directly contribute to tumorigenesis. In this study, we aimed to determine the status of intercellular junction proteins expression in JJ012 human malignant chondrosarcoma cells and investigate the effect of the antitumorigenic cytokine, proline-rich polypeptide-1 (PRP-1) on their expression. The cell junction pathway array data indicated downregulation of desmosomal proteins, such as desmoglein (1,428-fold), desmoplakin (620-fold) and plakoglobin (442-fold). The tight junction proteins claudin 11 and E-cadherin were also downregulated (399-and 52-fold, respectively). Among the upregulated proteins were the characteristic for tumors gap junction β-5 protein (connexin 31.1) and the pro-inflammatory pathway protein intercellular adhesion molecule (upregulated 129-and 43-fold, respectively). We demonstrated that PRP-1 restored the expression of the abovementioned downregulated in chondrosarcoma desmosomal proteins. PRP-1 inhibited H3K9-specific histone demethylase activity in chondrosarcoma cells in a dose-dependent manner (0.5 µg/ml PRP, 63%; 1 µg/ml PRP, 74%; and 10 µg/ml PRP, 91% inhibition). Members of the H3K9 family were shown to transcriptionally repress tumor suppressor genes and contribute to cancer progression. Our experimental data indicated that PRP-1 restores tumor suppressor desmosomal protein expression in JJ012 human chondrosarcoma cells and inhibits H3K9 demethylase activity, contributing to the suppression of tumorigenic potential in chondrosarcoma cells.

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Section: Introductionmentioning

confidence: 99%

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Galoian

Qureshi

Wideroff

et al. 2014

Molecular and Clinical Oncology

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“…На сегодняшний день МЭП описан в костных саркомах -хордоме, саркоме Юинга, хондросаркоме, остеосаркоме. МЭП в саркомах, являясь по существу важным биологическим и клиническим про-цессом, проявляется экспрессией молекулярных маркеров эпителиальной архитектуры -Е-Cadherin, Cytokeratin, EMA, Catenin, а также зачастую эпителиоидно-клеточной морфологией [38]. В исследовании M. Fitzgerald и соавт.…”

Section: Introductionunclassified

“…По данным J. Yang и соавт. (2014), саркома Юин-га экспрессирует Claudin-1 (tight junction protein), ZO-1, Occluding [38]. Остеосаркома экспрессирует Cadherin-11 (CDH11), AMF/PG1 [38].…”

Section: Introductionunclassified

“…(2014), саркома Юин-га экспрессирует Claudin-1 (tight junction protein), ZO-1, Occluding [38]. Остеосаркома экспрессирует Cadherin-11 (CDH11), AMF/PG1 [38]. В хондросаркоме экспрессиру-ются E-Cadherin, Desmocollin 3, Maspin, 14-3-3σ [38].…”

Section: Introductionunclassified

“…Остеосаркома экспрессирует Cadherin-11 (CDH11), AMF/PG1 [38]. В хондросаркоме экспрессиру-ются E-Cadherin, Desmocollin 3, Maspin, 14-3-3σ [38]. Мар-керы Cytokeratin, EMA, CD44, Е-Cadherin, Vascular cell adhesion molecule экспрессируются в хордоме [38].…”

Section: Introductionunclassified

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Lymph node metastasis of osteosarcomas

Vasiliev

2016

Arkh. patol.

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Первичные саркомы кости составляют менее 0,2% всех злокачественных опухолей человека [1,2]. Спектр нозологических форм костных процессов включает специ-фические злокачественные опухоли скелета, недиффе-ренцированные саркомы и мягкотканные саркомы -опухоли, гистогенетически типичные для мягких тканей. Специфические злокачественные опухоли объединяют остеосаркому, хондросаркому, саркому Юинга, адаман-тиному, хордому, злокачественную гигантоклеточную опухоль. Из них первые три опухоли в структуре заболева-емости костными саркомами составляют большинство -более 75% [1,2]. Частота встречаемости остеосаркомы, хондросаркомы и саркомы Юинга равна 35,1, 25,8 и 16% соответственно [1,2]. Мягкотканные саркомы чаще всего включают лейомиосаркому, ангиосаркому, синовиаль-ную саркому, липосаркому, злокачественную опухоль из оболочек периферических нервов [1, 2]. Метастазирова-ние костных сарком осуществляется преимущественно гематогенным путем -до 90% случаев [1]. Органом-ми-шенью для гематогенного метастаза являются, как прави-ло, легкие, реже -кости скелета, головной мозг [1][2][3]. Однако в малой части случаев метастазы поражают лим-фатические узлы. Метастазы в лимфатических узлах могут быть как солитарные, так и множественные [4,5]. Воз-можно метастатическое поражение не только «первого эшелона» лимфатической системы -регионарного аппа-рата, но и отдаленных групп лимфатических узлов, обна-руживаемых в средостении, забрюшинном пространстве, шее, парааортальной области [5][6][7]. Так, например, опи-саны метастазы остеосаркомы бедренной кости в лимфа-Васильев Николай

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A genetic dichotomy between pure sclerosing epithelioid fibrosarcoma (SEF) and hybrid SEF/low‐grade fibromyxoid sarcoma: A pathologic and molecular study of 18 cases

Prieto-Granada

Zhang

Chen

et al. 2014

Genes Chromosomes & Cancer

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Sclerosing epithelioid fibrosarcoma (SEF) is a rare soft tissue tumor exhibiting considerable morphologic overlap with low grade fibromyxoid sarcoma (LGFMS). Moreover, both SEF and LGFMS show MUC4 expression by immunohistochemistry. While the majority of LGFMS cases are characterized by a FUS-CREB3L1 fusion, both FUS-CREB3L2 and EWSR1-CREB3L1 fusions were recently demonstrated in a small number of LGFMS and SEF/LGFMS hybrid tumors. In contrast, recent studies pointed out that SEF harbor frequent EWSR1 rearrangements, with only a minority of cases showing FUS-CREB3L2 fusions. In an effort to further characterize the molecular characteristics of pure SEF and hybrid SEF/LGFMS lesions, we undertook a clinicopathologic, immunohistochemical and genetic analysis of a series of 10 SEF and 8 hybrid SEF/LGFMS tumors. The mortality rate was similar between the two groups, 44% within the pure SEF group and 37% in the hybrid SEF/LGFMS with a mean overall follow-up of 66 months. All but one pure SEF and all hybrid SEF/LGFMS tested cases showed MUC4 immunoreactivity. The majority (90%) of pure SEF cases showed EWSR1 gene rearrangements by FISH with only one case exhibiting FUS rearrangement. Of the 9 EWSR1 positive cases, 6 cases harbored CREB3L1 break-apart, two had CREB3L2 rearrangement (a previously unreported finding) and one lacked evidence of CREB3L1/2 abnormalities. In contrast, all hybrid SEF/LGFMS tumors exhibited FUS and CREB3L2 rearrangements. These results further demarcate a relative cytogenetic dichotomy between pure SEF, often characterized by EWSR1 rearrangements, and hybrid SEF/LGFMS, harboring FUS-CREB3L2 fusion; the latter group recapitulating the genotype of LGFMS.

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Mesenchymal to epithelial transition in sarcomas

Cited by 45 publications

References 47 publications

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Lymph node metastasis of osteosarcomas

A genetic dichotomy between pure sclerosing epithelioid fibrosarcoma (SEF) and hybrid SEF/low‐grade fibromyxoid sarcoma: A pathologic and molecular study of 18 cases

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