p68 DEAD Box RNA Helicase Expression in Keratinocytes

Kahlina, Kornelija; Goren, Itamar; Pfeilschifter, Josef; Frank, Stefan

doi:10.1074/jbc.m402467200

Cited by 32 publications

(12 citation statements)

References 49 publications

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“…The moderate reduction in the clonogenic survival of DQAD-p68 and also wt-p68 overexpressing cells may be attributable to the mislocation of p68 proteins to the nucleolus due to overexpression (see also 34) or inhibition of RNA polymerase II activity as reported by Andersen et al . (56).…”

Section: Discussionmentioning

confidence: 63%

“…Though it has been speculated that p68 is essential for cell proliferation (33,34), its efficient knock-down as well as that of p72/p82 (to ∼5 and 15% of the control, respectively; see Figure 1A) did only slightly alter the proliferation rate of HeLa cells (Figure 2A and B) and their distribution in G 1 , S and G 2 phases as revealed by flow cytometry (FACS) analysis (Figure 2C). In contrast, after co-suppression of all three DEAD box proteins, the proliferation of HeLa cells stopped (Figure 2A) and their DNA replication was blocked (data not shown).…”

Section: Resultsmentioning

confidence: 99%

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Redundant role of DEAD box proteins p68 (Ddx5) and p72/p82 (Ddx17) in ribosome biogenesis and cell proliferation

Jalal¹,

Uhlmann‐Schiffler²,

Stahl³

2007

Nucleic Acids Research

129

138

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The DEAD box proteins encoded by the genes ddx5 (p68) and ddx17 (isoforms p72 and p82) are more closely related to each other than to any other member of their family. We found that p68 negatively controls p72/p82 gene expression but not vice versa. Knocking down of either gene does not affect cell proliferation, in case of p68 suppression, however, only on condition that p72/p82 overexpression was granted. In contrast, co-silencing of both genes causes perturbation of nucleolar structure and cell death. In mutant studies, the apparently redundant role(s) of p68 and p72/p82 correspond to their ability to catalyze RNA rearrangement rather than RNA unwinding reactions. In search for possible physiological targets of this RNA rearrangement activity it is shown that the nucleolytic cleavage of 32S pre-rRNA is reduced after p68 subfamily knock-down, most probably due to a failure in the structural rearrangement process within the pre-60S ribosomal subunit preceding the processing of 32S pre-rRNA.

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Section: Discussionmentioning

confidence: 63%

Section: Resultsmentioning

confidence: 99%

Redundant role of DEAD box proteins p68 (Ddx5) and p72/p82 (Ddx17) in ribosome biogenesis and cell proliferation

Jalal¹,

Uhlmann‐Schiffler²,

Stahl³

2007

Nucleic Acids Research

129

138

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“…Indeed, the absence of Prep1 leads to increased Meis1 protein also in hematopoietic cells, and this level increases in the subsequent transplantations of the leukemic cells ( Figure 2 ). Increased Meis1 is bound to affect the self-renewal of transduced cells, since Meis1 quantitatively regulates the leukemic stem cell frequency [32], and the aggressiveness of the leukemias, as Meis1 regulates the latency of MLL leukemias [22]. Thus it is likely that the progressively higher level of Meis1 in the serial transplantations explains the increased serial replating efficiency, and the increased oncogenic potency.…”

Section: Discussionmentioning

confidence: 99%

The Deficiency of Tumor Suppressor Prep1 Accelerates the Onset of Meis1- Hoxa9 Leukemogenesis

et al. 2014

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Prep1 and Meis1 ortholog TALE transcription factors have opposing roles in tumorigenesis: Meis1 serves as an oncogene, Prep1 as a tumor suppressor. We now report that, Meis1 overexpression in primary Prep1-deficient (Prep1i/i) embryonic hematopoietic cells increases self-renewal potential of cells in vitro but not in vivo, whereas leukemia is instead obtained when Meis1 is combined with another oncogene, HoxA9. Prep1i/i Meis1-HoxA9-generated leukemic cells are less differentiated and grow more aggressively after the second passage in the mouse. These data indicate that Prep1 represents a barrier to the transforming activity of Meis1 in vitro, but its absence is not sufficient to induce early leukemogenesis. On the other hand, the Prep1i/i background appears to favor the insurgence of mutations that cause a more aggressive Meis1-HoxA9-generated leukemia. Indeed, the Prep1i/i leukemic cells upregulate the Polycomb protein Bmi-1 and expectedly down-regulate the Ink4a/Arf locus products. Finally, an important feature contributed by the Prep1i/i background is the post-transcriptional increase in Meis1 protein level.

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“…To date, increasing evidence shows that these DEAD family proteins are also involved in cell proliferation regulation and tumorigenesis. For example, a prototypic DEAD box RNA helicase, p68, was recently found to be induced during serum stimulation in NIH-3T3 fibroblasts (Stevenson et al, 1998) and keratinocytes (Kahlina et al, 2004), and is overexpressed in colorectal tumors (Causevic et al, 2001). This is rather different from DDX3 because this protein's expression is downregulated in liver tumors (see Figure 1 and Table 1) and a reduction in DDX3 expression promotes cell proliferation in NIH-3T3 cells ( Figure 5).…”

Section: Discussionmentioning

confidence: 99%

“…Although the DEAD box proteins share similar biological function, covering many aspects of RNA metabolism, they also play unique roles in other cellular processes, such as growth regulation and tumor development. For example, the p68 DEAD box RNA helicase has been shown to be involved in cell proliferation (Stevenson et al, 1998;Kahlina et al, 2004), and overexpression of several DEAD box proteins p68, rck/p54, and DDX1 has been found in tumors (Godbout et al, 1998;Nakagawa et al, 1999;Causevic et al, 2001). These are indicative of a relationship between DEAD box proteins and abnormal or proliferative disease.…”

Section: Introductionmentioning

confidence: 91%

DDX3, a DEAD box RNA helicase, is deregulated in hepatitis virus-associated hepatocellular carcinoma and is involved in cell growth control

Chang¹,

Chi²,

et al. 2005

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Hepatocellular carcinoma (HCC) is one of the leading causes of cancer deaths worldwide and is highly correlated with hepatitis virus infection. Our previous report shows that a DEAD box RNA helicase, DDX3, is targeted and regulated by hepatitis C virus (HCV) core protein, which implicates the involvement of DDX3 in HCV-related HCC development. In this study, the potential role of DDX3 in hepatocarcinogenesis is investigated by examining its expression in surgically excised human HCC specimens. Here we report the differential deregulation of DDX3 expression in hepatitis virus-associated HCC. A significant downregulation of DDX3 expression is found in HCCs from hepatitis B virus (HBV)-positive patients, but not from HCV-positive ones, compared to the corresponding nontumor tissues. The expression of DDX3 is differentially regulated by the gender and, moreover, there is a tendency that the downregulation of DDX3 expression in HCCs is more frequent in males than in females. Genetic knockdown of DDX3 with small interfering RNAs (siRNA) in a nontransformed mouse fibroblast cell line, NIH-3T3, results in a premature entry to S phase and an enhancement of cell growth. This enhanced cell cycle progression is linked to the upregulation of cyclin D1 and the downregulation of p21 WAF1 in the DDX3 knockdown cells. In addition, constitutive reduction of DDX3 expression increases the resistance of NIH-3T3 cells to serum depletion-induced apoptosis and enhances the ras-induced anchorage-independent growth, indicating the involvement of DDX3 in cell growth control. These findings together with the previous study suggest that the deregulation of DDX3, a DEAD box RNA helicase with cell growth-regulatory functions, is involved in HBV-and HCV-associated pathogenesis.

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p68 DEAD Box RNA Helicase Expression in Keratinocytes

Cited by 32 publications

References 49 publications

Redundant role of DEAD box proteins p68 (Ddx5) and p72/p82 (Ddx17) in ribosome biogenesis and cell proliferation

Redundant role of DEAD box proteins p68 (Ddx5) and p72/p82 (Ddx17) in ribosome biogenesis and cell proliferation

The Deficiency of Tumor Suppressor Prep1 Accelerates the Onset of Meis1- Hoxa9 Leukemogenesis

DDX3, a DEAD box RNA helicase, is deregulated in hepatitis virus-associated hepatocellular carcinoma and is involved in cell growth control

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