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Gene expression analysis of microtubule affinity-regulating kinase 2 in non-small cell lung cancer.

Marshall EA, Ng KW, Anderson C, Hubaux R, Thu KL, Lam WL, Martinez VD - Genom Data (2015)

Bottom Line: MARK2 is a serine/threonine-protein kinase, and is a key component in the phosphorylation of microtubule-associated proteins [2], [3].A recent study published by Hubaux et al. found that microtubule affinity-regulating kinase 2 (MARK2) showed highly frequent DNA and RNA level disruption in lung cancer cell lines and independent non-small cell lung cancer (NSCLC) cohorts [4].Furthermore, a microarray-based transcriptome analysis of three short hairpin RNA (shRNA)-mediated MARK2 knockdown lung adenocarcinoma cell lines (GEO#: GSE57966) revealed an association between MARK2 gene expression and cell cycle activation and DNA damage response.

View Article: PubMed Central - PubMed

Affiliation: Department of Integrative Oncology, BC Cancer Agency, Vancouver, Canada.

ABSTRACT
Lung cancer is the leading cause of cancer death worldwide, and has a five-year survival rate of 18% [1]. MARK2 is a serine/threonine-protein kinase, and is a key component in the phosphorylation of microtubule-associated proteins [2], [3]. A recent study published by Hubaux et al. found that microtubule affinity-regulating kinase 2 (MARK2) showed highly frequent DNA and RNA level disruption in lung cancer cell lines and independent non-small cell lung cancer (NSCLC) cohorts [4]. These alterations result in the acquisition of oncogenic properties in cell lines, such as increased viability and anchorage-independent growth. Furthermore, a microarray-based transcriptome analysis of three short hairpin RNA (shRNA)-mediated MARK2 knockdown lung adenocarcinoma cell lines (GEO#: GSE57966) revealed an association between MARK2 gene expression and cell cycle activation and DNA damage response. Here, we present a detailed description of transcriptome analysis to support the described role of MARK2 in promoting a malignant phenotype.

No MeSH data available.


Related in: MedlinePlus

Gene set enrichment analysis: A gene-set enrichment analysis (GSEA) was performed on differentially expressed genes between shRNA-MARK2 and controls. Two-fold change genes identified on NCI-H1993 (green), NCI-H1693 (blue) and NCI-H1650 (red) were chosen as inputs for A) Transcription factor targets or B) canonical pathways gene sets analysis. Negatively and positively enriched gene sets are shown in bars to the left and right of the zero line. A q-value ≤ 0.05 was used a significance threshold. Names of significantly enriched gene sets are shown on the y-axis.
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f0020: Gene set enrichment analysis: A gene-set enrichment analysis (GSEA) was performed on differentially expressed genes between shRNA-MARK2 and controls. Two-fold change genes identified on NCI-H1993 (green), NCI-H1693 (blue) and NCI-H1650 (red) were chosen as inputs for A) Transcription factor targets or B) canonical pathways gene sets analysis. Negatively and positively enriched gene sets are shown in bars to the left and right of the zero line. A q-value ≤ 0.05 was used a significance threshold. Names of significantly enriched gene sets are shown on the y-axis.

Mentions: The C3.TFT (Transcription Factor Targets) and C2.CP (Canonical Pathways) collection from the Molecular Signatures Database (MSigDB) were selected to preferentially acquire information from canonical pathway and transcription factor target gene sets in each cell line. In cell line and tumor analysis, fifty-six gene sets were be significantly enriched. This cohort includes genes associated with NF-κB, DNA repair, E2F, and Myc/Max. Additionally, negative association between NF-κB and MARK2 expression has been previously observed (Fig. 4).


Gene expression analysis of microtubule affinity-regulating kinase 2 in non-small cell lung cancer.

Marshall EA, Ng KW, Anderson C, Hubaux R, Thu KL, Lam WL, Martinez VD - Genom Data (2015)

Gene set enrichment analysis: A gene-set enrichment analysis (GSEA) was performed on differentially expressed genes between shRNA-MARK2 and controls. Two-fold change genes identified on NCI-H1993 (green), NCI-H1693 (blue) and NCI-H1650 (red) were chosen as inputs for A) Transcription factor targets or B) canonical pathways gene sets analysis. Negatively and positively enriched gene sets are shown in bars to the left and right of the zero line. A q-value ≤ 0.05 was used a significance threshold. Names of significantly enriched gene sets are shown on the y-axis.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664690&req=5

f0020: Gene set enrichment analysis: A gene-set enrichment analysis (GSEA) was performed on differentially expressed genes between shRNA-MARK2 and controls. Two-fold change genes identified on NCI-H1993 (green), NCI-H1693 (blue) and NCI-H1650 (red) were chosen as inputs for A) Transcription factor targets or B) canonical pathways gene sets analysis. Negatively and positively enriched gene sets are shown in bars to the left and right of the zero line. A q-value ≤ 0.05 was used a significance threshold. Names of significantly enriched gene sets are shown on the y-axis.
Mentions: The C3.TFT (Transcription Factor Targets) and C2.CP (Canonical Pathways) collection from the Molecular Signatures Database (MSigDB) were selected to preferentially acquire information from canonical pathway and transcription factor target gene sets in each cell line. In cell line and tumor analysis, fifty-six gene sets were be significantly enriched. This cohort includes genes associated with NF-κB, DNA repair, E2F, and Myc/Max. Additionally, negative association between NF-κB and MARK2 expression has been previously observed (Fig. 4).

Bottom Line: MARK2 is a serine/threonine-protein kinase, and is a key component in the phosphorylation of microtubule-associated proteins [2], [3].A recent study published by Hubaux et al. found that microtubule affinity-regulating kinase 2 (MARK2) showed highly frequent DNA and RNA level disruption in lung cancer cell lines and independent non-small cell lung cancer (NSCLC) cohorts [4].Furthermore, a microarray-based transcriptome analysis of three short hairpin RNA (shRNA)-mediated MARK2 knockdown lung adenocarcinoma cell lines (GEO#: GSE57966) revealed an association between MARK2 gene expression and cell cycle activation and DNA damage response.

View Article: PubMed Central - PubMed

Affiliation: Department of Integrative Oncology, BC Cancer Agency, Vancouver, Canada.

ABSTRACT
Lung cancer is the leading cause of cancer death worldwide, and has a five-year survival rate of 18% [1]. MARK2 is a serine/threonine-protein kinase, and is a key component in the phosphorylation of microtubule-associated proteins [2], [3]. A recent study published by Hubaux et al. found that microtubule affinity-regulating kinase 2 (MARK2) showed highly frequent DNA and RNA level disruption in lung cancer cell lines and independent non-small cell lung cancer (NSCLC) cohorts [4]. These alterations result in the acquisition of oncogenic properties in cell lines, such as increased viability and anchorage-independent growth. Furthermore, a microarray-based transcriptome analysis of three short hairpin RNA (shRNA)-mediated MARK2 knockdown lung adenocarcinoma cell lines (GEO#: GSE57966) revealed an association between MARK2 gene expression and cell cycle activation and DNA damage response. Here, we present a detailed description of transcriptome analysis to support the described role of MARK2 in promoting a malignant phenotype.

No MeSH data available.


Related in: MedlinePlus