Alteration in gene expression profile and biological behavior in human lung cancer cell line NL9980 by nm23-H1 gene silencing

Ma, Wei; Chen, Jun; Xue, Xingyang; Wang, Zhuomin; Liu, Hongyu; Wang, Ting; Bai, Yun; Tang, Shou‐Ching; Zhou, Qinghua

doi:10.1016/j.bbrc.2008.04.083

Cited by 24 publications

(26 citation statements)

References 23 publications

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“…Some transfection investigations have demonstrated several biochemical effects of NME1 knockdown on tumor cellular functions, such as cell motility (Ma et al 2008). In our study, we have investigated for the first time the functional mechanism of the metastasis suppressor NME1 at the maternal-fetal interface in humans.…”

Section: Discussionmentioning

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

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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: Discussionmentioning

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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“…Human Genome U133 Plus 2.0 microarrays with 54,000 probe sets were purchased from Affymetrix (Santa Clara, CA, USA), and microarray assays were performed as previously described. 7 For significant gene expression changes, (Log 2 Signal Ratio) ≥1 were considered to be upregulated, and (Log 2 Signal Ratio) ≤1 were considered to be downregulated.…”

Section: Methodsmentioning

confidence: 99%

Gene silencing of BAG-1 modulates apoptotic genes and sensitizes lung cancer cell lines to cisplatin-induced apoptosis

Liu

Liang²,

Liu

et al. 2010

Cancer Biology & Therapy

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“…Multiple transfection experiments indicate that, when nm23-H1 expression is forcibly restored, metastases to the lungs, lymph nodes and other organs significantly decreased (30). On the other hand, evidence indicates that the MMPs are down-regulated in cells expressing relatively higher levels of nm23-H1 (31). The molecular mechanism of nm23-H1 in suppressing lung cancer invasion and metastasis may be through the regulation of the differential expression of a series of tumor metastasis-associated genes.…”

Section: Discussionmentioning

confidence: 99%

Effect of Fraxiparine, a type of low molecular weight heparin, on the invasion and metastasis of lung adenocarcinoma A549 cells

Chen

Ye²,

Feng³

et al. 2010

Oncology Letters

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Abstract. Lung cancer is one of the most highly malignant tumors, and a significant threat to human health. Lung cancer patients often exhibit tumor cell invasion and metastasis, which often render current treatments ineffective. Recently, the beneficial effects of low molecular weight heparin (LMWH) on cancer metastasis were reported in pre-clinical research studies. LMWH may be a potential drug for cancer therapy. However, the mechanism of LMWH on the invasion and metastasis of cancer has yet to be determined. This study investigated the effects of Fraxiparine on the proliferation, invasion and metastasis of the human lung adenocarcinoma A549 cell line. MTT assay and flow cytometry showed that Fraxiparine slightly inhibited the cell viability dose-and timedependently, but did not arrest the A549 cells in the G1 phase nor induce early apoptosis. The transwell chamber assay showed that Fraxiparine significantly suppressed the invasion and migration of the A549 cells in vitro. Fraxiparine also markedly inhibited the adhesion of the A549 cells to Matrigel. The RT-PCR assay demonstrated that the reduction in invasion and metastasis may be related to the up-regulation of nm23-H1 and the down-regulation of the heparanase expression. Moreover, the RT-PCR assay and Western blot analysis demonstrated that down-regulation of the expression of integrin β1 and β3, as well as that of matrix metalloproteinase-2 and -9 may be responsible for the inhibition of the invasion and metastasis of A549 cells by Fraxiparine.

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Alteration in gene expression profile and biological behavior in human lung cancer cell line NL9980 by nm23-H1 gene silencing

Cited by 24 publications

References 23 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

Gene silencing of BAG-1 modulates apoptotic genes and sensitizes lung cancer cell lines to cisplatin-induced apoptosis

Effect of Fraxiparine, a type of low molecular weight heparin, on the invasion and metastasis of lung adenocarcinoma A549 cells

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