Limits...
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

Principal component analysis. A PCA analysis was performed on normalized intensity values on NCI-H1650 (red), NCI-H1693 (blue) and NCI-H1993 (green). The experimental conditions (knock-down — triangles and pLKO controls, squares) are shown.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4664690&req=5

f0015: Principal component analysis. A PCA analysis was performed on normalized intensity values on NCI-H1650 (red), NCI-H1693 (blue) and NCI-H1993 (green). The experimental conditions (knock-down — triangles and pLKO controls, squares) are shown.

Mentions: A principal component analysis (PCA) was performed on RMA normalized expression data. First, the analysis reveled that biological replicates showed a high degree of correlation for each cell line. The NCI-H1650 MARK2-KD experiments clustered further apart from PLKO control in the PCA graph, suggesting that the knockdown of MARK2 had the strongest effect in this cell line. In NCI-H1693 and NCI-H1993 MARK2, knockdown cell lines are closely related to their respective control counterparts (Fig. 3).


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)

Principal component analysis. A PCA analysis was performed on normalized intensity values on NCI-H1650 (red), NCI-H1693 (blue) and NCI-H1993 (green). The experimental conditions (knock-down — triangles and pLKO controls, squares) are shown.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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

f0015: Principal component analysis. A PCA analysis was performed on normalized intensity values on NCI-H1650 (red), NCI-H1693 (blue) and NCI-H1993 (green). The experimental conditions (knock-down — triangles and pLKO controls, squares) are shown.
Mentions: A principal component analysis (PCA) was performed on RMA normalized expression data. First, the analysis reveled that biological replicates showed a high degree of correlation for each cell line. The NCI-H1650 MARK2-KD experiments clustered further apart from PLKO control in the PCA graph, suggesting that the knockdown of MARK2 had the strongest effect in this cell line. In NCI-H1693 and NCI-H1993 MARK2, knockdown cell lines are closely related to their respective control counterparts (Fig. 3).

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