Résumé
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.
Langue d'origine | English |
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Pages (de-à) | 145-148 |
Nombre de pages | 4 |
Journal | Genomics Data |
Volume | 6 |
DOI | |
Statut de publication | Published - déc. 15 2015 |
Publié à l'externe | Oui |
Note bibliographique
Funding Information:This work was supported by grants from the Canadian Institutes for Health Research (CIHR) ( MOP-97839 and MOP-123273 ). E.A.M. and C.A. are supported by a BC Cancer Studentship , C.A. by CBCF Studentship , K.L.T. by Vanier Canada Scholarship .
Publisher Copyright:
© 2015 The Authors.
ASJC Scopus Subject Areas
- Biotechnology
- Biochemistry
- Molecular Medicine
- Genetics
PubMed: MeSH publication types
- Journal Article