The clinical value of serum hepatocyte growth factor levels in patients undergoing primary radiotherapy for glioma: effect on progression-free survival

Liang, Qingle; Mo, Zheng-ying; Wang, Ping; Li, Xiao; Liu, Zhixiang; Zhou, Zhang-Ming

doi:10.1007/s12032-014-0122-5

Cited by 9 publications

(3 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have documented that HGF is overexpressed in gliomas, and high-grade gliomas express more HGF than lower-grade astrocytomas. Serum HGF influenced progression-free survival [16]. SiBMK1/U87 cells showed dramatically decreased invasive ability compared with SCR/U87 cells (Fig.…”

Section: Bmk1 Promoted Glioma Cell Invasionmentioning

confidence: 96%

miR-429 inhibits glioma invasion through BMK1 suppression

et al. 2015

View full text Add to dashboard Cite

The purpose of this research was to examine the relationship between big mitogen-activated protein kinase 1 (BMK1) and miRNA miR-429 and to determine the effect of miR-429 on glioma invasiveness. Immunohistochemistry was used to evaluate BMK1 expression in glioma tissues. Real-time PCR was used to measure the expression of miR-429 and other RNAs. Western blot was used to detect the expression of BMK1 and other related proteins. Wound healing, Matrigel invasion, and chemotaxis assays were performed to detect the invasion and migration of glioma cell lines. The actual binding site of miR-429 to the 3' untranslated region of BMK1 was confirmed by luciferase assay and RNA immunoprecipitation. BMK1 expression was associated with the World Health Organization grading of glioma and inversely correlated with patient survival. Suppression of BMK1 inhibited the migration and invasion of glioma cells by interfering with mesenchymal transition. Additionally, hepatocyte growth factor-induced GSK3β phosphorylation was suppressed through BMK1 knockdown. Interestingly, our findings validated a novel role for miR-429 in suppressing the migration and invasion of glioma by directly inhibiting BMK1 expression. We also found that miR-429 expression in glioma cells and tissues was lower than that in normal cells and adjacent non-neoplastic tissues, and miR-429 overexpression inhibited invasive activity of glioma cells both in vitro and in vivo. Furthermore, our data validated that miR-429 downregulation was due to the hypermethylation of its promoter region. Our results indicated that BMK1 modulation by miR-429 has an important function in glioma invasion both in vitro and in vivo.

show abstract

Section: Bmk1 Promoted Glioma Cell Invasionmentioning

confidence: 96%

miR-429 inhibits glioma invasion through BMK1 suppression

et al. 2015

View full text Add to dashboard Cite

show abstract

“…HGF inhibition is as effective as standard chemotherapy in inhibiting local tumor growth [45]. The fact that the concentration of these factors is high in the peripheral region of glioblastoma multiform, which is a strong brain tumor with advanced invasion skills, supports the view that they play a role in motility [46].…”

Section: Ecm's Invasion and The Stages Of Invasionmentioning

confidence: 98%

Is Extracellular Matrix a Castle Against to Invasion of Cancer Cells?

Altınay¹

2016

Tumor Metastasis

View full text Add to dashboard Cite

Metastasis is a complicated course that involves the spread of a neoplasm to distant parts of the body from its original site. A cancer cell must complete a series of steps before it becomes a clinically detectable lesion for successful colonization in the body. These are separation from the primary tumor, invasion and penetration of their basement membranes, entry into the blood vessels and survival within blood, and entry into lymphatics. A major challenge in extracellular matrix (ECM) biology is to understand the roles of the ECM and how disruption of ECM dynamics may contribute to cancer. A noteworthy area of forthcoming cancer research will be to determine whether abnormal ECM could be an effective cancer therapeutic target. We should understand how ECM composition and organization are normally maintained and how they may be deregulated in cancer. So the aims of this chapter were to focus on extracellular matrix. Invasion and metastatic skills, properties and functions of the ECM, abnormal ECM dynamics, tumor microenvironment and ECM, details of ECM invasion, role of ECM and ECM-associated proteins in metastasis, tumor dormant and metastatic process, essential component of the niches, role of the ECM in tumor angiogenesis and lymphangiogenesis are be briefly explained in this chapter.

show abstract

“…Activation of the HGF/c-MET pathway has been evaluated using serum or plasma HGF, because HGF is expelled from tumor cells to the extracellular matrix and blood plasma by a paracrine mechanism [ 12 ]. Increased serum HGF (sHGF) has been reported to be a negative prognostic marker in various malignancies including colorectal cancer, gastric cancer [ 13 – 15 ], prostate cancer [ 16 ], ovarian cancer [ 17 ], breast cancer [ 18 , 19 ], glioma[ 20 ], melanoma [ 21 ], and multiple myeloma [ 22 , 23 ]. Recently, a Spanish group reported that high sHGF in patients with SCLC predicts poor outcome and epithelial-mesenchymal transition (EMT) change in the tumor [ 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

Clinical impact of high serum hepatocyte growth factor in advanced non-small cell lung cancer

et al. 2017

View full text Add to dashboard Cite

Activation of c-MET through hepatocyte growth factor (HGF) increases tumorigenesis, induces resistance, and is associated with poor prognosis in various solid tumors. However, the clinical value of serum HGF (sHGF) in patients with advanced non-small cell lung cancer (NSCLC), especially those receiving cytotoxic chemotherapy, remains unknown. Here, we show that sHGF may be useful to predict tumor response and progression-free survival (PFS) in patients with advanced NSCLC. A total of 81 patients with NSCLC were investigated. sHGF levels were evaluated using ELISA at 4 time-points: at pre-treatment, at response-evaluation (1–2 months after treatment initiation), at the best tumor response, and at disease progression. As a control biomarker, CEA was also evaluated in lung adenocarcinoma. Positive-sHGF at response-evaluation predicted poor PFS compared with Negative-sHGF in both first-line (median, 153.5 vs. 288.0; P < 0.05) and second-line treatment (87.0 vs. 219.5; P = 0.01). In 55 patients that received cytotoxic chemotherapy, multiple Cox proportional hazards models showed significant independent associations between poor PFS and Positive-sHGF at response-evaluation (hazard ratio, 4.24; 95% CI, 2.05 to 9.46; P < 0.01). Lung adenocarcinoma subgroup analysis showed that in patients receiving second cytotoxic chemotherapy, there were no significant differences in PFS between patients with low-CEA compared with those with high-CEA, but Positive-sHGF at pre-treatment or at response-evaluation predicted poor PFS (35.0 vs. 132.0; P < 0.01, 50.0 vs. 215.0; P < 0.01, respectively). These findings give a rationale for future research investigating the merit of sHGF as a potential clinical biomarker to evaluate HGF/c-MET activity, which would be useful to indicate administration of c-MET inhibitors.

show abstract

The clinical value of serum hepatocyte growth factor levels in patients undergoing primary radiotherapy for glioma: effect on progression-free survival

Cited by 9 publications

References 31 publications

miR-429 inhibits glioma invasion through BMK1 suppression

miR-429 inhibits glioma invasion through BMK1 suppression

Is Extracellular Matrix a Castle Against to Invasion of Cancer Cells?

Clinical impact of high serum hepatocyte growth factor in advanced non-small cell lung cancer

Contact Info

Product

Resources

About