Hepatocyte Growth Factor/Scatter Factor Is Implicated in the Mode of Stromal Invasion of Uterine Squamous Cervical Cancer

Shimabukuro, Koji; Ichinose, Shizuko; Koike, Ryuji; Kubota, Toshiro; Yamaguchi, Masahiko; Miyasaka, Masayuki; Asô, Takeshi

doi:10.1006/gyno.2001.6347

Cited by 25 publications

(21 citation statements)

References 39 publications

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“…In human cancers, overexpression of c-Met correlates well with metastatic progression or a poor clinical outcome in patients with carcinoma of the breast [18], stomach [19], endometrium [20], liver [21], colorectum [22], thyroid [23], prostate [24], kidney [25], or urinary bladder [26]. In cervical cancer, expression of c-met mRNA has been seen in both SKG-IIIa (squamous cell carcinoma) and HeLa-S3 (adenocarcinoma) cell lines [27]. One study [28] found that c-Met overexpression positively correlated with local recurrence and overall survival (OS) for 94 patients with cervical cancer, including 10 patients with adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

The significance of prohibitin and c-Met/hepatocyte growth factor receptor in the progression of cervical adenocarcinoma

et al. 2006

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Section: Introductionmentioning

confidence: 99%

The significance of prohibitin and c-Met/hepatocyte growth factor receptor in the progression of cervical adenocarcinoma

et al. 2006

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“…This stimulus was also sufficient for glioblastoma A172 cells. HeLa cells invade in response to growth factor gradients (27). Baseline invasion rates of f10% were observed in response to epidermal growth factor (EGF, Peprotech, Rocky Hill, NJ).…”

Section: Introductionmentioning

confidence: 99%

PEA-15 Inhibits Tumor Cell Invasion by Binding to Extracellular Signal-Regulated Kinase 1/2

et al. 2007

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Phosphoprotein enriched in astrocytes of 15 kDa (PEA-15) binds to extracellular signal-regulated kinase 1 and 2 (ERK1/2) mitogen-activated protein (MAP) kinases to alter ERK1/2 cellular localization and target preferences and binds to adaptors in the extrinsic cell death pathway to block apoptosis. Here, we report that PEA-15 protein expression is inversely correlated with the invasive behavior of breast cancer in an immunohistochemical analysis of a breast cancer progression tissue microarray. Short hairpin RNA-mediated inhibition of PEA-15 expression increased the invasion of PEA-15-expressing tumor cells in vitro, suggesting a causative role for PEA-15 in the inhibition of invasion. This causative role was confirmed by the finding that the enforced expression of PEA-15 in invasive tumor cells reduced invasion. The effect of PEA-15 on tumor invasion is mediated by its interaction with ERK1/2 as shown by the following: (a) PEA-15 mutants that fail to bind ERK1/2 did not inhibit invasion; (b) overexpression of ERK1 or activated MAP/ERK kinase (MEK) reversed the inhibitory effect of PEA-15; (c) when an inhibitor of ERK1/2 activation reduced invasion, PEA-15 expression did not significantly reduce invasion further. Furthermore, we find that the effect of PEA-15 on invasion seems to relate to the nuclear localization of activated ERK1/2. PEA-15 inhibits invasion by keeping ERK out of the nucleus, as a PEA-15 mutant that cannot prevent ERK nuclear localization was not able to inhibit invasion. In addition, membrane-localized ERK1, which sequesters endogenous ERK1 to prevent its nuclear localization, also inhibited invasion. These results reveal that PEA-15 regulates cancer cell invasion via its ability to bind ERK1/2 and indicate that nuclear entry of ERK1/2 is important in tumor behavior. [Cancer Res 2007;67(4):1536-44]

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“…In the mouse, estradiol modulates the expression of HGF in the ovary during ovarian cancer (25). Another critical consideration is that increased HGF levels are associated with increased tumor aggressiveness in uterine squamous cervical cancer (26). HGF secretion by stromal fibroblasts is increased in certain ovarian (27) and cervical tumors (26).…”

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confidence: 99%

“…Another critical consideration is that increased HGF levels are associated with increased tumor aggressiveness in uterine squamous cervical cancer (26). HGF secretion by stromal fibroblasts is increased in certain ovarian (27) and cervical tumors (26). Understanding how estradiol affects HGF in breast and FRT tumors is critical to a complete understanding of these pathologies.…”

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confidence: 99%

Estradiol modulation of hepatocyte growth factor by stromal fibroblasts in the female reproductive tract

Coleman

Wright

Ghosh

et al. 2009

Fertility and Sterility

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Hepatocyte Growth Factor/Scatter Factor Is Implicated in the Mode of Stromal Invasion of Uterine Squamous Cervical Cancer

Cited by 25 publications

References 39 publications

The significance of prohibitin and c-Met/hepatocyte growth factor receptor in the progression of cervical adenocarcinoma

The significance of prohibitin and c-Met/hepatocyte growth factor receptor in the progression of cervical adenocarcinoma

PEA-15 Inhibits Tumor Cell Invasion by Binding to Extracellular Signal-Regulated Kinase 1/2

Estradiol modulation of hepatocyte growth factor by stromal fibroblasts in the female reproductive tract

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