RGD Reference Report - Ectopic doublecortin gene expression suppresses the malignant phenotype in glioblastoma cells. - Rat Genome Database

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Ectopic doublecortin gene expression suppresses the malignant phenotype in glioblastoma cells.

Authors: Santra, Manoranjan  Zhang, Xuepeng  Santra, Sutapa  Jiang, Feng  Chopp, Michael 
Citation: Santra M, etal., Cancer Res. 2006 Dec 15;66(24):11726-35.
RGD ID: 12904748
Pubmed: PMID:17178868   (View Abstract at PubMed)
DOI: DOI:10.1158/0008-5472.CAN-06-1978   (Journal Full-text)

Doublecortin (DCX) is one of the three genes found from Affymetrix gene chip analysis related to glioma patient survival. Two other genes (e.g., osteonectin and semaphorin 3B) are well characterized as antioncogenic and tumor suppressor genes. However, there is no report about the involvement of DCX in cancer. Here, we show that gene transfer technology into DCX-deficient glioblastoma cell lines, such as A172, U87, U251N, RG2, and 9L, with DCX cDNA significantly suppressed growth of these glioma cells. U87 cells with ectopic expression of DCX exhibit a marked suppression of the transformed phenotype as growth arrested in the G(2) phase of the cell cycle progression, small colony formation in soft agar, and no tumor formation in nude rats. This transformed phenotype can be restored by knocking down DCX expression with DCX small interfering RNA. DCX was highly phosphorylated in glioma cells. Phosphorylation in the glioma cells was greater than in noncancer cells such as mouse NIH 3T3 and human embryonic kidney 293T cells. Coimmunoprecipitation of the phosphorylated DCX and spinophilin/neurabin II from DCX-synthesizing glioma cells indicated their interaction. This interaction would lead to a block of anchorage-independent growth as neurabin II is a synergistic inhibitor of anchorage-independent growth with p14ARF (ARF). Interaction between phosphorylated DCX and neurabin II may induce the association of the protein phosphatase 1 catalytic subunit (PP1) with neurabin II and inactivate PP1 and block mitosis during G(2) and M phases of the cell cycle progression. Thus, DCX seems to be a tumor suppressor of glioma.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
high grade glioma  ISODcx (Mus musculus)12904748; 12904748 RGD 
high grade glioma  IMP 12904748 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Dcx  (doublecortin)

Genes (Mus musculus)
Dcx  (doublecortin)

Genes (Homo sapiens)
DCX  (doublecortin)


Additional Information