Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcriptional profiling by array of human head and neck squamous cell carcinoma to study the correlation between galectin-1 upregulation and the presence of SMA positive cancer-associated fibroblasts

ABSTRACT: In this study, we set the presence of smooth muscle actin (SMA)-positive cancer-associated fibroblasts (CAFs) in relation to galectin-1 and its in vivo competitor (galectin-3). In squamous cell carcinomas of head and neck, upregulation of galectin-1 presence is highly significantly correlated to presence of smooth muscle actin-positive cancer-associated fibroblasts in the tumor. In order to pinpoint correlations on the molecular level, we applied microarray analyses to the transcription profiles of the corresponding tumors. Significant correlations of several transcripts were detected with the protein level of galectin-1 in the cancer-associated fibroblasts.

ORGANISM(S): Homo sapiens

SUBMITTER: Michal Kolar

PROVIDER: E-MTAB-850 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Smooth muscle actin-expressing stromal fibroblasts in head and neck squamous cell carcinoma: increased expression of galectin-1 and induction of poor prognosis factors.

Valach Jaroslav J Fík Zdeněk Z Strnad Hynek H Chovanec Martin M Plzák Jan J Cada Zdeněk Z Szabo Pavol P Sáchová Jana J Hroudová Miluše M Urbanová Markéta M Steffl Martin M Pačes Jan J Mazánek Jiří J Vlček Cestmír C Betka Jan J Kaltner Herbert H André Sabine S Gabius Hans-Joachim HJ Kodet Roman R Smetana Karel K Gál Peter P Kolář Michal M

International journal of cancer 20120409 11

Tumor stroma is an active part influencing the biological properties of malignancies via molecular cross-talk. Cancer-associated fibroblasts play a significant role in this interaction. These cells frequently express smooth muscle actin and can be classified as myofibroblasts. The adhesion/growth-regulatory lectin galectin-1 is an effector for their generation. In our study, we set the presence of smooth muscle actin-positive cancer-associated fibroblasts in relation to this endogenous lectin an ...[more]

PMID: 22447203

Similar Datasets

Project description:Radiation and chemotherapy represent standard-of-care cancer treatments, however most treated patients eventually experience tumor recurrence, treatment failure and metastatic dissemination with fatal consequences. To elucidate molecular mechanisms of resistance to radio- and chemo-therapy, we exposed human cancer cell lines (HeLa, MCF-7, and DU145) to clinically relevant doses of 5-azacytidine or ionizing radiation and compared the transcript profiles of all surviving cell subpopulations including non-adherent fraction. Stress-mobilized non-adherent cell fractions differed from other survivors in deregulation of hundreds of genes including those involved in interferon response. Exposure of cancer cells to interferon-gamma but not interferon-beta resulted in development of a heterogeneous non-adherent fraction comprising, besides apoptotic/necrotic cells, also live cells featuring active Notch signaling and expressing stem cell markers. Interferon-gamma-mediated loss of adhesion and anoikis-resistance required active Erk pathway interlinked with interferon signaling by IRF1, as chemical inhibition of MEK or siRNA-mediated knockdown of Erk1/2 and IRF1 prevented mobilization of the surviving non-adherent population. Noteworthy, among the top scoring genes upregulated in surviving non-adherent tumor cells induced by 5-azacytidine or irradiation was a skin-specific protein suprabasin (SBSN), a recently identified oncoprotein. SBSN expression required the activity of the MEK/Erk pathway, and siRNA-mediated knockdown of SBSN resulted in suppression of the non-adherent fraction in irradiated, interferon-gamma- and 5-azacytidine-treated cells, respectively. Consistently, ectopic expression of SBSN isoforms enhanced the non-adherent phenotype, suggesting functional participation of SBSN in genotoxic stress-induced phenotypic plasticity and stress resistance. The stress-induced expression of skin protein(s) in a subset of cancer cells indicates partial induction of a keratinocyte-like expression program. Overall, we propose that IFN and Erk signaling drive the heterogeneous response of cancer cells to genotoxic therapies and expression of keratinocyte-specific genes as key players in mobilization and survival of cancer stem-like cells, with implications for cancer evolution and therapy resistance.

Dataset Information

Transcriptional profiling by array of human head and neck squamous cell carcinoma to study the correlation between galectin-1 upregulation and the presence of SMA positive cancer-associated fibroblasts

Publications

Smooth muscle actin-expressing stromal fibroblasts in head and neck squamous cell carcinoma: increased expression of galectin-1 and induction of poor prognosis factors.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure