Expression profiling of invasion associated molecules in head and neck cancer cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE143689 | GEO | 2023/01/15
REPOSITORIES: GEO
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Project description:Introduction: Metastasis of breast cancer is the main cause of death in patients. Previous genome-wide studies have identified gene expression patterns correlated with cancer patient outcome, however these were mostly derived from whole tissue without respect to cell heterogeneity. In reality, only a small subpopulation of migratory and invasive cells inside the primary tumor is responsible for escaping and initiating dissemination and metastasis. When whole tissue is used for molecular profiling, the expression pattern of these cells is masked by the majority of the non-invasive tumor cells. Therefore, little information is available about the crucial early steps of the metastatic cascade: migration, invasion and entry of tumor cells into the systemic circulation. Method: In the past, we have developed an in vivo invasion assay which can capture specifically the highly motile tumor cells in the act of migrating inside living tumors (Wyckoff et al., 2004, Cancer Research). Here, we used this assay in orthotopic xenografts of human MDA-MB-231 breast cancer cells to selectively isolate the invasive cell subpopulation of the primary tumor. We then performed microarray analysis to compare the gene expression profile of these invading tumor cells to the average primary tumor cells. In this way, we derived a gene signature specific to breast cancer migration and invasion in vivo. Each sample of invasive (INV) and average primary tumor cells (APTC) was pooled from two tumor-bearing mice. RNA was extracted, made into cDNA, then amplified with the Clontech SMART amplification kit. Human reference RNA (Clontech) was amplified with identifical protocol. Each sample was then hybridized in a 28K Human cDNA microarray chip, custom printed from Albert Einstein College of Medicine (http://microarray1k.aecom.yu.edu/). Four replicates were used per group (Invasive vs. Average Primary Tumor).
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Project description:Elevated expression and activity of the epidermal growth factor receptor (EGFR) is associated with development and progression of head and neck cancer (HNC) and a poor prognosis. Clinical trials with EGFR tyrosine kinase inhibitors (TKIs; eg. erlotinib) have been disappointing in HNC. To investigate the mechanisms mediating resistance to these agents, we developed a HNC cell line (HN5-ER) with acquired erlotinib resistance. In contrast to parental HN5 HNC cells, HN5-ER cells exhibited an epithelial-mesenchymal (EMT) phenotype with increased migratory potential, reduced E-cadherin and epithelial-associated miRNAs, and elevated vimentin expression. Phosphorylated RTK profiling identified Axl activation in HN5-ER cells. Growth and migration of HN5-ER cells was blocked with a specific Axl inhibitor, R428, and R428 re-sensitized HN5-ER cells to erlotinib. Microarray analysis of HN5-ER cells confirmed the EMT phenotype associated with acquired erlotinib resistance, and identified activation of gene expression associated with cell migration and inflammation pathways. Moreover, increased expression and secretion of interleukin (IL)-6 and IL-8 in HN5-ER cells suggested a role for inflammatory cytokine signaling in EMT and erlotinib resistance. Expression of the tumor suppressor miR-34a was reduced in HN5-ER cells and increasing its expression abrogated Axl expression and reversed erlotinib resistance. Finally, analysis of 302 HNC patients revealed that high tumor Axl mRNA expression was associated with poorer survival (HR 1.66, p=0.007). In summary, our results identify Axl as a key mediator of acquired erlotinib resistance in HNC and suggest that therapeutic inhibition of Axl by small molecule drugs or specific miRNAs might overcome anti-EGFR therapy resistance. Differential gene expression between parental and acquired erlotinib resistant head and neck cancer cell lines of HN5.
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