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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

Comparison of raw vs. normalized probe intensity. Box-and-whisker plot of A) raw and B) log2 RMA normalized intensity data. Samples are in the following order: 1) NCI-H1650 pLKO control (Replicate 1), 2) NCI-H1650 MARK2 Knockdown (Replicate 1), 3) NCI-H1693 pLKO control (Replicate 1), 4) NCI-H1693 Mark2 Knockdown (Replicate 1), 5) NCI-H1993 pLKO control (Replicate 1), 6) NCI-H1993 Mark2 Knockdown (Replicate 1), 7) NCI-H1650 Mark2 Knockdown (Replicate 2), 8) NCI-H1650 pLKO control (Replicate 2), 9) NCI-H1693 pLKO control (Replicate 2), 10) NCI-H1693 Mark2 Knockdown (Replicate 2), 11) NCI-H1993 pLKO control (Replicate 2), 12) NCI-H1993 Mark2 Knockdown (Replicate 2).
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f0005: Comparison of raw vs. normalized probe intensity. Box-and-whisker plot of A) raw and B) log2 RMA normalized intensity data. Samples are in the following order: 1) NCI-H1650 pLKO control (Replicate 1), 2) NCI-H1650 MARK2 Knockdown (Replicate 1), 3) NCI-H1693 pLKO control (Replicate 1), 4) NCI-H1693 Mark2 Knockdown (Replicate 1), 5) NCI-H1993 pLKO control (Replicate 1), 6) NCI-H1993 Mark2 Knockdown (Replicate 1), 7) NCI-H1650 Mark2 Knockdown (Replicate 2), 8) NCI-H1650 pLKO control (Replicate 2), 9) NCI-H1693 pLKO control (Replicate 2), 10) NCI-H1693 Mark2 Knockdown (Replicate 2), 11) NCI-H1993 pLKO control (Replicate 2), 12) NCI-H1993 Mark2 Knockdown (Replicate 2).

Mentions: Probe cell intensity (.CEL) files were imported and normalized using the Robust Multiarray Averaging (RMA) normalization method [6]. Normalized probe intensities were summarized in order to display probe-level signal data. Signal intensity before and after log2 RMA signal transformation is displayed in Fig. 1. Distribution of probe intensity values was also assessed, confirming that log2-transformed normalized data is closer to a normal distribution (Fig. 2).


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)

Comparison of raw vs. normalized probe intensity. Box-and-whisker plot of A) raw and B) log2 RMA normalized intensity data. Samples are in the following order: 1) NCI-H1650 pLKO control (Replicate 1), 2) NCI-H1650 MARK2 Knockdown (Replicate 1), 3) NCI-H1693 pLKO control (Replicate 1), 4) NCI-H1693 Mark2 Knockdown (Replicate 1), 5) NCI-H1993 pLKO control (Replicate 1), 6) NCI-H1993 Mark2 Knockdown (Replicate 1), 7) NCI-H1650 Mark2 Knockdown (Replicate 2), 8) NCI-H1650 pLKO control (Replicate 2), 9) NCI-H1693 pLKO control (Replicate 2), 10) NCI-H1693 Mark2 Knockdown (Replicate 2), 11) NCI-H1993 pLKO control (Replicate 2), 12) NCI-H1993 Mark2 Knockdown (Replicate 2).
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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

f0005: Comparison of raw vs. normalized probe intensity. Box-and-whisker plot of A) raw and B) log2 RMA normalized intensity data. Samples are in the following order: 1) NCI-H1650 pLKO control (Replicate 1), 2) NCI-H1650 MARK2 Knockdown (Replicate 1), 3) NCI-H1693 pLKO control (Replicate 1), 4) NCI-H1693 Mark2 Knockdown (Replicate 1), 5) NCI-H1993 pLKO control (Replicate 1), 6) NCI-H1993 Mark2 Knockdown (Replicate 1), 7) NCI-H1650 Mark2 Knockdown (Replicate 2), 8) NCI-H1650 pLKO control (Replicate 2), 9) NCI-H1693 pLKO control (Replicate 2), 10) NCI-H1693 Mark2 Knockdown (Replicate 2), 11) NCI-H1993 pLKO control (Replicate 2), 12) NCI-H1993 Mark2 Knockdown (Replicate 2).
Mentions: Probe cell intensity (.CEL) files were imported and normalized using the Robust Multiarray Averaging (RMA) normalization method [6]. Normalized probe intensities were summarized in order to display probe-level signal data. Signal intensity before and after log2 RMA signal transformation is displayed in Fig. 1. Distribution of probe intensity values was also assessed, confirming that log2-transformed normalized data is closer to a normal distribution (Fig. 2).

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