Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression array analysis of the hepatocyte growth factor (HGF) invasive program

ABSTRACT: HGF stimulates mitogenesis, motogenesis and morphogenesis in most epithelial target cells. Selective inhibition of HGF signaling blocks spontaneous metastasis, but not primary tumor growth, in the prostate adenocarcinoma derived PC3M cell xenograft model. To identify the HGF activated genes and pathways that contribute to cell motility and invasion, i.e. the HGF invasive program, expression profiling was performed on PC3M cells that were untreated or were treated with human HGF (hHGF), which drives all 3 primary activities, or with human HGF/NK2 (hNK2) or murine HGF (mHGF), which drive motility and invasion but not proliferation in human cells. Differences in gene expression profiles among these four groups were used to distiniguish between events associated with invasion (resulting from hNK2 or mHGF treatment) from those associated with the combination of invasion and proliferation (resulting from hHGF treatment). PC3M cells were left untreated or treated with hHGF, hNK2 or mHGF for 8, 16 or 32 hours prior to RNA extraction, cDNA preparation and array hybridization.

ORGANISM(S): Homo sapiens

SUBMITTER: Donald Bottaro

PROVIDER: E-GEOD-71404 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Expression array analysis of the hepatocyte growth factor invasive program.

Cecchi Fabiola F Lih Chih-Jian CJ Lee Young H YH Walsh William W Rabe Daniel C DC Williams Paul M PM Bottaro Donald P DP

Clinical & experimental metastasis 20150801 7

Signaling by human hepatocyte growth factor (hHGF) via its cell surface receptor (MET) drives mitogenesis, motogenesis and morphogenesis in a wide spectrum of target cell types and embryologic, developmental and homeostatic contexts. Oncogenic pathway activation also contributes to tumorigenesis and cancer progression, including tumor angiogenesis and metastasis, in several prevalent malignancies. The HGF gene encodes full-length hHGF and two truncated isoforms known as NK1 and NK2. NK1 induces ...[more]

PMID: 26231668

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Project description:The hepatocyte growth factor (HGF)/c-Met signaling pathway is known to mediate vascularization. We have previously demonstrated that expression of a human HGF transgene in the small airways produced mice (HGF TG) that were more susceptible to the tobacco carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). We also have observed that HGF TG mice display significantly enhanced vascularization in the lungs that increases over time compared to wild-type (WT) littermates. To analyze which genes might contribute to increased vascularization from HGF overexpression in the airways, RNA and protein were isolated from whole lungs of individual HGF TG and WT adult mice. We profiled the mRNA expression of several hundred genes representative of six biological pathways involved in transformation, angiogenesis, and tumorigenesis using two commercial microarrays. Significant changes in expression over a 1.5-fold boundary were also observed in lung tumors derived from NNK-treated HGF TG mice. Lung tumors were induced by exposing mice to four weekly i.p. injections of 3mg NNK (15μg/μl) over 2 weeks. Whole lungs from control untreated animals were dissected after sacrifice at 10, 20, or 40 wks of age, and NNK induced lung tumors were dissected from the animals at 20 or 40 weeks of age. Total RNA was extracted from whole lung or isolated tumors from HGF TG or WT mice using TRIzol reagent and the Array Grade Total RNA Isolation Kit. The cDNA was generated and labeled using the TrueLabeling-AMP Linear RNA Amplication Kit. RNA was analyzed from 28 mice in total. The angiogenesis array was used to analyze 10 samples taken from 40 week old mice (HGF TG untreated [n=4], WT untreated [n=4], HGF TG NNK treated [n=1], WT NNK treated [n=1]) and 6 samples from 20 week old mice (HGF TG untreated [n=2], WT untreated [n=2], HGF TG NNK treated [n=1], WT NNK treated [n=1]). The cancer gene array was used to analyze 8 samples taken from 40 week old mice (HGF TG untreated [n=2], WT untreated [n=2], HGF TG NNK treated [n=2], WT NNK treated [n=2]) and 4 samples from 20 week old mice (HGF TG untreated [n=2], WT untreated [n=2]).

Dataset Information

Expression array analysis of the hepatocyte growth factor (HGF) invasive program

Publications

Expression array analysis of the hepatocyte growth factor invasive program.

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