Gestational trophoblastic neoplasms (GTNs) do not display epithelial-to-mesenchymal transition (EMT) features

Dubruc, Estelle; Allias, Fabienne; Morel, Anne; Golfier, François; Puisieux, Alain; Devouassoux‐Shisheboran, Mojgan

doi:10.1007/s00428-019-02551-7

Cited by 3 publications

(1 citation statement)

References 12 publications

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“…Few studies on epithelial-to-mesenchymal transition in choriocarcinoma cells have been published. One study even suggests that gestational trophoblastic neoplasms do not display EMT features [21].…”

Section: Mir-373-3p Targets Tgfβr2 Which Influences Emt In Choriocarmentioning

confidence: 99%

miR-373-3p inhibits EMT via regulation of TGFβR2 in choriocarcinoma

Zuo

et al. 2020

Preprint

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Background: Previous studies have indicated that early metastasis is a major cause of mortality in patients with choriocarcinoma. However, what determines whether early metastasis of choriocarcinoma has occurred is unknown. The emerging role of miRNA in regulating cancer development and progression has been recognized. MiR-373 has been shown to play pivotal roles in tumorigenesis and metastasis. However, whether miR-373 functions to promote choriocarcinoma metastasis is not clear. The purpose of this study is to determine the function of miR-373-3p in the progression of this cancer. Methods: In this study, we first compared epithelial-to-mesenchymal transition (EMT)-related markers, which were inversely correlated with miR-373-3p expression, in trophoblast and choriocarcinoma cell lines. Using PCR and Western blot, upregulation of miR-373-3p was observed to inhibit EMT progression. Similarly, gain- and loss-of-function studies revealed that ectopic miR-373-3p overexpression inhibited the metastasis of choriocarcinoma cells. Results: Our results revealed that miR-373-3p acted as an EMT inhibitor in JEG-3 and JAR cells; this was due to its mediation of the TGF-β signalling pathway, which was responsible for EMT. Bioinformatic analysis demonstrated that miR-373-3p interacted with the 3' untranslated region of TGFβR2 mRNA, and then Western blot and dualluciferase reporter gene assays verified this interaction. Conclusions: Our findings suggest that miR-373-3p upregulation partly accounts for TGFβR2 downregulation and leads to a restraint of EMT and metastasis. MiR-373-3p may therefore serve as a valuable potential target in the treatment of choriocarcinoma.

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Section: Mir-373-3p Targets Tgfβr2 Which Influences Emt In Choriocarmentioning

confidence: 99%

miR-373-3p inhibits EMT via regulation of TGFβR2 in choriocarcinoma

Zuo

et al. 2020

Preprint

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Molecular Analyses of Chorionic-Type Intermediate Trophoblastic Lesions: Atypical Placental Site Nodules are Closer to Placental Site Nodules Than Epithelioid Trophoblastic Tumors

et al. 2023

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Molecular analyses of chorionic-type intermediate trophoblastic lesions: Atypical placental site nodules are closer to placental site nodules than epithelioid trophoblastic tumors

Jeremie

Allias

Trécourt

et al. 2022

Preprint

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Gestational trophoblastic diseases derived from the chorionic-type intermediate trophoblast include benign placental site nodule (PSN) and malignant epithelioid trophoblastic tumor (ETT). Among PSN, the WHO classification introduced a new entity named atypical placental site nodule (APSN), corresponding to an ETT precursor, for which the diagnostic criteria remain unclear, leading to a risk of over-diagnosis and difficulties in patient management. We retrospectively studied 8 PSN, 7 APSN and 8 ETT to better characterize this new entity. We performed an immunohistochemical analysis (p63, hPL, Cyclin E, and Ki67), a transcriptional analysis using the Nanostring method to quantify the expression of 760 genes involved in the main tumorigenesis pathways, and a RNA sequencing to identify fusion transcripts. The immunohistochemical analysis did not reveal any significant difference in Cyclin E expression between the three groups (p = 0.476), whereas the Ki67 index was significantly (p < 0.001) higher in ETT compared to APSN and PSN samples. None of the APSN samples harbored the LPCAT1-TERT fusion transcripts previously reported in ETT. The transcriptomic analysis allowed robust clustering of ETT distinct from the APSN/PSN group but failed to distinguish APSN from PSN. Indeed, only seven genes were differentially-expressed between PSN and APSN samples, CCL19 upregulation and EPCAM downregulation were the most discriminating features of APSN. In contrast, 80 genes discriminated ETT from APSN, establishing a molecular signature for ETT. Gene set analysis identified significant enrichments in the DNA damage repair, immortality and stemness, and cell cycle signaling pathways when comparing ETT and APSN. These results suggested that APSN might not represent a distinct entity but rather a variant of PSN or a transitional stage between PSN and ETT. RNA sequencing and the transcriptional signature of ETT described herein could serve as triage for APSN from curettage or biopsy material, enabling the identification of the cases that need further clinical investigations.

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Gestational trophoblastic neoplasms (GTNs) do not display epithelial-to-mesenchymal transition (EMT) features

Cited by 3 publications

References 12 publications

miR-373-3p inhibits EMT via regulation of TGFβR2 in choriocarcinoma

miR-373-3p inhibits EMT via regulation of TGFβR2 in choriocarcinoma

Molecular Analyses of Chorionic-Type Intermediate Trophoblastic Lesions: Atypical Placental Site Nodules are Closer to Placental Site Nodules Than Epithelioid Trophoblastic Tumors

Molecular analyses of chorionic-type intermediate trophoblastic lesions: Atypical placental site nodules are closer to placental site nodules than epithelioid trophoblastic tumors

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