Adhesion-related proteins E-cadherin, P-cadherin, CD44, and CD44v6, and antimetastatic protein nm23H1 in complete hydatidiform moles in relation to invasion potential

Balaram, Prabha; Alex, Swapna; Panikkar, Beena; Rajalekshmi, T N

doi:10.1111/j.1048-891x.2004.014316.x

Cited by 14 publications

(12 citation statements)

References 26 publications

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“…The previous study has proved that the MAPK/ERK1/2 signaling pathway is involved in modulation of invasion and migration of human trophoblasts (McKinnon et al 2001, Balaram et al 2004, Qiu et al 2004, Wu et al 2004, Huang et al 2006. In the present study, the BeWo cells with NME1 silencing were treated with U0126 NME1 at the human maternal-fetal interface (30 mmol/l) or vehicle for 30, 60, and 90 min.…”

Section: Nme1 Silencing Improves Trophoblast Invasiveness Mainly Thromentioning

confidence: 74%

“…Nometastatic gene 23-H1 (NME1, also known as nm23-H1) is a classical tumor metastasis suppressor gene. A correlation of increased NME1 expression to low metastatic potential of cancer cells has been established in several malignancies, based on tumor prognostic and transfection studies (Ouatas et al 2003, Balaram et al 2004, Ferenc et al 2004, Sirotkovic-Skerlev et al 2005, Tee et al 2006. In the trophoblastic disease, the expression of NME1 is closely relative to the prognosis, and thus can be used as a reference indicator to evaluate the tumor progress (Balaram et al 2004).…”

Section: Introductionmentioning

confidence: 99%

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NME1 at the human maternal–fetal interface downregulates titin expression and invasiveness of trophoblast cells via MAPK pathway in early pregnancy

Xie

Hou²,

Li³

et al. 2010

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Nometastatic gene 23-H1 (NME1, also known as nm23-H1) is a wide-spectrum tumor metastasis suppressor gene that plays an important role in suppressing the invasion and metastasis of tumor cells. It has been demonstrated that NME1 is also expressed in human firsttrimester placenta, but its function at maternal-fetal interface is not clear. The present study aimed to elucidate the biological function of NME1 at the maternal-fetal interface, especially on invasion of the human extravillous cytotrophoblasts (EVCTs). NME1 has been identified in both human trophoblast cells and decidual stromal cells (DSCs) in early pregnancy. We have proved that NME1 silencing in vitro increases the titin protein translation in the invasive EVCTs. Moreover, NME1 can inactivate the phospho-extracellular signalregulated kinase 1/2 (P-ERK1/2) in trophoblasts in a time-dependent manner, and U0126, an inhibitor of MAPK/ERK, can inhibit partly the enhanced invasiveness and titin expression in trophoblasts induced by NME1 silencing. Interestingly, the expression of NME1 in either villi or decidua is higher significantly in miscarriage than that of the normal early pregnancy. These findings first reveal that the NME1 expressed in trophoblasts and DSCs controls the inappropriate invasion of human first-trimester trophoblast cells via MAPK/ERK1/2 signal pathway, and the overexpression of NME1 at maternal-fetal interface leads to pregnancy wastage.

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Section: Nme1 Silencing Improves Trophoblast Invasiveness Mainly Thromentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

NME1 at the human maternal–fetal interface downregulates titin expression and invasiveness of trophoblast cells via MAPK pathway in early pregnancy

Xie

Hou²,

Li³

et al. 2010

Reproduction

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“…We found signiWcantly lower PPM1A protein expression in human placenta villi at the Wrst trimester compared with that at term by Western blot and IHC. HM is a gestational trophoblastic disease which is prone to malignant transformation and has the potential to develop into invasive carcinoma (Altieri et al 2003;Balaram et al 2004;Knoeller et al 2003;Sebire et al 2001). …”

Section: Discussionmentioning

confidence: 99%

Protein phosphatase 1A (PPM1A) is involved in human cytotrophoblast cell invasion and migration

Zhang

Zhou

Lin

et al. 2009

Histochem Cell Biol

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Trophoblast invasion is crucial for embryo implantation and placentation. Excessive trophoblast invasion leads to hydatidiform moles and choriocarcinoma. PPM1A is a phosphatase which dephosphorylates and inactivates a broad range of substrates, including TGF-beta, MAP kinases, p38 and JNK kinase cascades, and is involved in tumor suppression. The objective of this study was to investigate the expression of PPM1A in normal and malignant human placenta and its role in trophoblast invasion, which shares many similarities with invasion of tumor cells. By Western blotting and immunocytochemistry, significantly higher expression of PPM1A in human placental villi at term was found as compared with that during the first trimester. Furthermore, the expression level of PPM1A protein in hydatidiform moles was lower compared with that during normal pregnancy. We further investigated the function of PPM1A in extravillous trophoblast cell line HTR8/SVneo. Transwell migration and Matrigel invasion assays demonstrated that PPM1A siRNA significantly promoted the motility and invasiveness of the cells. Gelatin zymography showed that knockdown of PPM1A with siRNA elevated the expression of pro-matrix metalloproteinase pro-(MMP)-9, but down-regulated tissue inhibitors of metalloproteinases (TIMP)-2. The present data indicate that PPM1A plays a critical role in the regulation of normal placentation by inhibiting trophoblast migration and invasion.

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“…[16], with some immunoreactivity still detectable at term [32]. VE-cad (cadherin-5) has a similar distribution [16].…”

Section: Classical Cadherinsmentioning

confidence: 99%

Adhesion Molecules in Human Trophoblast – A Review. I. Villous Trophoblast

Aplin¹,

Jones²,

Harris³

2009

Placenta

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In the placental villus, cells attach to basement membrane via integrin α6β4 and adhere both laterally and apically to their neighbours. The most prominent adhesive specialisation seen in the electron microscope is the desmosome, which connects cytotrophoblast cells (CTB) laterally and also contributes to the attachment of CTB to the overlying syncytium.However, numerous cadherins and other junctional proteins are also present in the corresponding plasma membrane domains, indicating a multiplicity of adhesive interactions.Integrins, tight junction components and cadherins are all found in the syncytial microvillous membrane, perhaps reflecting its ability to form intersyncytial bridges. There is a wide gulf to be filled between molecular anatomy and functional studies, with much to be learned about the role of adhesion molecules in regulating villous epithelial integrity, homeostasis and growth.3

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Adhesion-related proteins E-cadherin, P-cadherin, CD44, and CD44v6, and antimetastatic protein nm23H1 in complete hydatidiform moles in relation to invasion potential

Cited by 14 publications

References 26 publications

NME1 at the human maternal–fetal interface downregulates titin expression and invasiveness of trophoblast cells via MAPK pathway in early pregnancy

NME1 at the human maternal–fetal interface downregulates titin expression and invasiveness of trophoblast cells via MAPK pathway in early pregnancy

Protein phosphatase 1A (PPM1A) is involved in human cytotrophoblast cell invasion and migration

Adhesion Molecules in Human Trophoblast – A Review. I. Villous Trophoblast

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