Tumor necrosis factor α promotes invasiveness of cholangiocarcinoma cells via its receptor, TNFR2

Tanimura, Yoko; Kokuryo, Toshio; Tsunoda, Nobuyuki; Yamazaki, Yukiko; Oda, Koji; Nimura, Yuji; Mon, Naing Naing; Huang, Pengyu; Nakanuma, Yasuni; Chen, Min-Fu; Jan, Yi-Yin; Yeh, Ta-Sen; Chiu, Cheng-Taug; Hsieh, Ling–Ling; Hamaguchi, Michinari

doi:10.1016/j.canlet.2004.07.027

Cited by 52 publications

(55 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…25 Among many inflammatory cytokines, TNF-a has been proposed as an important, endogenous tumor promoter. [28][29][30] TNF-a can activate cell growth and stimulate the production of MMP9 in CC. 29,30 In addition, multiple intracellular signaling, such as NF-kb, MAP kinases, PI3K, and focal adhesion kinase (FAK), may be involved in TNF-a-dependent MMP9 secretion in CC.…”

Section: Discussionmentioning

confidence: 99%

“…[28][29][30] TNF-a can activate cell growth and stimulate the production of MMP9 in CC. 29,30 In addition, multiple intracellular signaling, such as NF-kb, MAP kinases, PI3K, and focal adhesion kinase (FAK), may be involved in TNF-a-dependent MMP9 secretion in CC. 29,30,36 TNF-a is in turn controlled in the tumor environment by various factors such as other cytokines.…”

Section: Discussionmentioning

confidence: 99%

“…29,30 In addition, multiple intracellular signaling, such as NF-kb, MAP kinases, PI3K, and focal adhesion kinase (FAK), may be involved in TNF-a-dependent MMP9 secretion in CC. 29,30,36 TNF-a is in turn controlled in the tumor environment by various factors such as other cytokines. 26,27 In addition, TNF-a can regulate several intracellular signaling and transcriptional factors.…”

Section: Discussionmentioning

confidence: 99%

“…Tanimura et al reported that TNF-a can activate tumor invasion through the production of MMP9. 29,30 Multiple intracellular signaling, such as mitogen-activated protein kinase ((MAPK) or phosphatidylinositol 3-kinase (PI3K), were involved in TNF-a-dependent MMP9 secretion in CC; 29 however, detailed molecular mechanisms of TNF-a-dependent MMP9 secretion in CC has not been fully elucidated.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Fascin is involved in tumor necrosis factor-α-dependent production of MMP9 in cholangiocarcinoma

Onodera

Zen

Harada

et al. 2009

Laboratory Investigation

Self Cite

View full text Add to dashboard Cite

Fascin is an actin-binding protein involved in the cell motility. Recently, aberrant expression of fascin in carcinoma cells was reported to participate in their invasive growth in cooperation with proteinases such as matrix metalloproteinases (MMPs). This study examined the participation of fascin in the progression of cholangiocarcinoma (CC) with reference to MMPs and tumor necrosis factor-a (TNF-a). Expression levels of fascin and MMP2 and 9 were examined immunohistochemically in human non-neoplastic biliary epithelium (13 cases) and CC (87 cases). The relationship between fascin and MMP9-expression levels was examined using two CC cell lines (CCKS-1 and HuCCT1). It was also examined whether or not fascin was involved in TNF-a-induced overproduction of MMP9 in CC. Fascin and MMP9 were expressed in 49 and 53% of CC samples, respectively, and the expression of these genes was frequent in intrahepatic CC. Fascin expression was correlated significantly with MMP9 expression. In particular, these two molecules were expressed more intensely at the invasive fronts of CC. Fascin expression was an unfavorable prognostic factor for patients with intrahepatic CC. In vitro studies showed that TNF-a could induce the overexpression of fascin and MMP9 in two CC cell lines. A knockdown study of fascin by siRNA showed that TNF-a induced the overproduction of fascin, which in turn upregulated MMP9 expression. Overexpression of fascin may have an important function in the progression of CC, and fascin expression might be involved in the signaling pathway in TNF-a-dependent production of MMP9 in CC.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Fascin is involved in tumor necrosis factor-α-dependent production of MMP9 in cholangiocarcinoma

Onodera

Zen

Harada

et al. 2009

Laboratory Investigation

Self Cite

View full text Add to dashboard Cite

show abstract

“…In addition, TNF-α was able to induce the expression of MMP9, largely related with tumor invasiveness in CCA [81,82].…”

Section: Transforming-growth Factor-β (Tgf-β)-dependent Signaling Is mentioning

confidence: 98%

Epithelial-mesenchymal transition in cholangiocarcinoma: From clinical evidence to regulatory networks

Vaquero

Guedj

Clapéron

et al. 2017

Journal of Hepatology

113

122

View full text Add to dashboard Cite

Cholangiocarcinoma (CCA) is an aggressive tumor with a poor prognosis due to its late clinical presentation and the lack of effective non-surgical therapies. Unfortunately, most of the patients are not eligible for curative surgery owing to the presence of metastases at the time of diagnosis. Therefore, it is important to understand the steps leading to cell dissemination in patients with CCA. To metastasize from the primary site, cancer cells must acquire migratory and invasive properties by a cell plasticity-promoting phenomenon known as epithelial-mesenchymal transition (EMT). EMT is a reversible dynamic process by which epithelial cells gradually adopt structural and functional characteristics of mesenchymal cells, and has lately become a center of attention in the field of metastatic dissemination. In the present review, we aim to provide an extensive overview of the current clinical data and the prognostic value of different EMT markers that have been analyzed in CCA. We summarize all the regulatory networks implicated in EMT from the membrane receptors to the main EMT-inducing transcription factors (SNAIL, TWIST and ZEB). Furthermore, since a tumor is a complex structure not exclusively formed by tumor cells, we also address the prominent role of the main cell types of the desmoplastic stroma that characterizes CCA in the regulation of EMT. Finally, we discuss the therapeutic considerations and difficulties faced to develop an effective anti-EMT treatment due to the redundancies and bypasses among the pathways regulating EMT. 4Key Point Box -EMT is an early event of metastasis that endows tumor cells with invasive properties enabling them to spread toward other territories.-EMT contributes to CCA progression and chemoresistance.-The three families of transcription factors that regulate epithelial and mesenchymal marker expression during EMT (SNAIL, TWIST and ZEB) contribute to CCA progression.-Cells of CCA microenvironment, and not only cancer cells, lead to the activation of EMT.

show abstract

The Tumor Microenvironment in Cholangiocarcinoma Progression

et al. 2020

View full text Add to dashboard Cite

Tumor necrosis factor α promotes invasiveness of cholangiocarcinoma cells via its receptor, TNFR2

Cited by 52 publications

References 25 publications

Fascin is involved in tumor necrosis factor-α-dependent production of MMP9 in cholangiocarcinoma

Fascin is involved in tumor necrosis factor-α-dependent production of MMP9 in cholangiocarcinoma

Epithelial-mesenchymal transition in cholangiocarcinoma: From clinical evidence to regulatory networks

The Tumor Microenvironment in Cholangiocarcinoma Progression

Contact Info

Product

Resources

About