ArticlePathology oncology research : POR2012
HGF/c-Met overexpressions, but not met mutation, correlates with progression of non-small cell lung cancer.
Article in Pathology oncology research : POR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 51 citations in OpenAlex.
- B7-H3 and c-MET in advanced prostate cancer: exploring possibilities of novel bi-specific drug development.European journal of medical research · 2025Article
- The Impact ofJournal of Cancer · 2025Article
- RhoA and vigilin are candidates for immunohistochemical markers for epithelioid malignant mesothelioma.Scientific reports · 2022Article
- c-Met: A Promising Therapeutic Target in Bladder Cancer.Cancer management and research · 2022Review
- Receptor Tyrosine Kinases and Their Signaling Pathways as Therapeutic Targets of Curcumin in Cancer.Frontiers in pharmacology · 2021Review
- Membrane receptor activation mechanisms and transmembrane peptide tools to elucidate them.The Journal of biological chemistry · 2020Review
- Met is involved in TIGAR-regulated metastasis of non-small-cell lung cancer.Molecular cancer · 2018Article
- Curcumin inhibited HGF-induced EMT and angiogenesis through regulating c-Met dependent PI3K/Akt/mTOR signaling pathways in lung cancer.Molecular therapy oncolytics · 2016Article
- Coexpression of c-Met and Notch-1 correlates with poor prognosis in resected non-small-cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Overexpression of P21-activated kinase 4 is associated with poor prognosis in non-small cell lung cancer and promotes migration and invasion.Journal of experimental & clinical cancer research : CR · 2015Article
- Association Analysis of MET Gene Polymorphism with Papillary Thyroid Carcinoma in a Chinese Population.International journal of endocrinology · 2015Article
- Clinical Trials in Non-Small Cell Lung Cancer with Biomarker-Driven Treatment Allocation: Ready or Not, Here We Come.Critical reviews in oncogenesis · 2015Review
- [Dysregulation of HGF/c-Met signal pathway and their targeting drugs in lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2014Review
- Expression of MACC1 and c-Met in human gastric cancer and its clinical significance.Cancer cell international · 2013Article
- Overexpression of metastasis-associated in colon cancer-1 associated with poor prognosis in patients with esophageal cancer.Pathology oncology research : POR · 2013Article
- A novel c-Met inhibitor, MK8033, synergizes with carboplatin plus paclitaxel to inhibit ovarian cancer cell growth.Oncology reports · 2013Article
- MicroRNA-449a is downregulated in non-small cell lung cancer and inhibits migration and invasion by targeting c-Met.PloS one · 2013Article
- Epigenetic upregulation of HGF and c-Met drives metastasis in hepatocellular carcinoma.PloS one · 2013Article
- Expression of HGF and Met in human tissues of colorectal cancers: biological and clinical implications for synchronous liver metastasis.International journal of medical sciences · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocyte Growth Factor (HGF) and its receptor c-Met are suggested to play an important role in progression of solid organ tumors by mediating cell motility, invasion and metastasis. Overexpression of HGF and c-Met have been shown in non-small-cell lung cancer (NSCLC). However, their role in tumor progression is not clearly defined. The aim of this study is to determine the role of HGF/c-Met pathway and its association with invasion related markers and clinicopathologic parameters in NSCLC. Immunohistochemical analysis was performed on 63 paraffin-embedded NSCLC tumor sections. The expressions of invasion related markers such as Matrix Metalloproteinases (MMPs) 2 and 9, Tissue Inhibitor Metalloproteinase (TIMP) 1 and 3 and RhoA were also examined. Co-expression of HGF/c-Met was significantly associated with lymph node invasion and TIMP-3 and RhoA overexpressions. There were positive correlation between TIMP-3 overexpression and advanced stage and negative correlation between RhoA overexpression and survival. DNA sequencing for Met mutations in both nonkinase and tyrosine kinase (TK) domain was established. A single nucleotide polymorphism (SNP) in sema domain and two SNPs in TK domain of c-Met were found. There was no statistically significant correlation between the presence of c-Met alterations and clinicopathologic parameters except shorter survival time in cases with two SNPs in TK domain. These results suggest that HGF/c-Met might exert their effects in tumor progression in association with RhoA and probably with TIMP-3. The blockade of the HGF/c-Met pathway with RhoA and/or TIMP-3 inhibitors may be an effective therapeutic target for NSCLC treatment.
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