Comparison of the effects of recombinant adenovirus-mediated expression of wild-type p53 and p27Kip1 on cell cycle and apoptosis in SUDHL-1 cells derived from anaplastic large cell lymphoma

Turturro, Francesco; Frist, Audrey Y.; Arnold, Marilyn D.; Pal, Asmita; Cook, Gregory A.; Seth, Prem

doi:10.1038/sj.leu.2402181

Cited by 8 publications

(10 citation statements)

References 27 publications

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“…[17][18][19] For the first time, we showed that adenovirus-mediated p27 Kip1 expression was able to induce in vitro apoptosis in SUDHL-1 cells derived from t(2:5)-ALCL. 20, 21 We also demonstrated that the effects of adenovirus-mediated p27 Kip1 expression were cell dependent and differed from the effects of adenovirus-mediated p53 expression in SUDHL-1 cells. 20 22 On the contrary, cells derived from HD were resistant to apoptosis induced by the same recombinant adenoviruses.…”

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 70%

“…In fact, other investigators and we have recently elucidated this concept in studies that will be discussed. 12,15,[20][21][22] In one study, we showed that the recombinant adenovirusmediated expression of exogenous p27 Kip1 was equally efficient in the cytoplasm and in the nucleus of SUDHL-1 and KARPAS 299 cells derived from t(2;5)-ALCL. 20 The presence of CAR and integrins on the cell surface of SUDHL-1 (Ref.…”

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

“…15 Furthermore, we recently showed that the level of apoptosis and the chronology of the event are correlated with the type of cytotoxic gene that is expressed by the recombinant adenovirus in the same cell line. 21 In fact, we analyzed the differences in cell cycle and apoptosis induced by the recombinant adenovirus-mediated expression of p53 or p27 Kip1 in SUDHL-1 cells. 21 The cytotoxic effect of the recombinant-mediated expression of p27 Kip1 was moi-dependent and it varied from cytostasis (prolonged G1 arrest of the cell cycle) at lower moi to frank apoptosis at higher moi of adenovirus.…”

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

“…21 In fact, we analyzed the differences in cell cycle and apoptosis induced by the recombinant adenovirus-mediated expression of p53 or p27 Kip1 in SUDHL-1 cells. 21 The cytotoxic effect of the recombinant-mediated expression of p27 Kip1 was moi-dependent and it varied from cytostasis (prolonged G1 arrest of the cell cycle) at lower moi to frank apoptosis at higher moi of adenovirus. 21 The dose-dependent dual effect of cytostasis/apoptois has been confirmed in a recent study, where we analyzed the effects of recombinant adenoviruses-mediated expression of p27 Kip1 , p21 WAF1 or p16 INK4A in SUDHL-1 cells.…”

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

“…21 The cytotoxic effect of the recombinant-mediated expression of p27 Kip1 was moi-dependent and it varied from cytostasis (prolonged G1 arrest of the cell cycle) at lower moi to frank apoptosis at higher moi of adenovirus. 21 The dose-dependent dual effect of cytostasis/apoptois has been confirmed in a recent study, where we analyzed the effects of recombinant adenoviruses-mediated expression of p27 Kip1 , p21 WAF1 or p16 INK4A in SUDHL-1 cells. 22 The past, the present and the future: infectivity of the lymphoid-derived cells and targeting the virion…”

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

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Recombinant adenovirus-mediated cytotoxic gene therapy of lymphoproliferative disorders: is CAR important for the vector to ride?

Turturro

2003

Gene Ther

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The literature has seen an incredible booming of publications related to the use of recombinant adenoviruses as therapeutic tools for lymphoproliferative disorders over the last decade. Several approaches of adenovirus-mediated gene expression have been used to transfect cell lines that are derived from lymphoid tumors and would have otherwise been refractory to other transfection methods. The identification of high-affinity receptor for human adenoviruses serotype 2 and 5, the coxsackie-adenovirus receptor (CAR), has raised the question about its relevance for the efficacy of recombinant adenovirus-mediated gene therapy. We review published studies that have analyzed the use of recombinant adenovirus vectors expressing cytotoxic genes for gene therapy in lymphomas, chronic lymphocytic leukemia and multiple myeloma. For simplicity, we group all these diseases under the term lymphoproliferative disorders. We analyze the use of recombinant adenovirus-mediated cytotoxicity by assessing the importance of the biochemical and intrinsic signaling pathways interacting with the products of the exogenous viral-mediated expression. Ultimately, we discuss studies that have been finalized to by-pass the limitations of the biodistribution of CAR by modifying or targeting adenovirus to other membrane proteins in cells derived from lymphoproliferative disorders.

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Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 70%

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

Section: Adenovirus-mediated Gene Therapy For Lymphoproliferative Dismentioning

confidence: 99%

See 3 more Smart Citations

Recombinant adenovirus-mediated cytotoxic gene therapy of lymphoproliferative disorders: is CAR important for the vector to ride?

Turturro

2003

Gene Ther

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Anaplastic lymphoma kinase proteins in growth control and cancer

Pulford

Morris

Turturro

2004

Journal Cellular Physiology

207

181

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The normal functions of full-length anaplastic lymphoma kinase (ALK) remain to be completely elucidated. Although considered to be important in neural development, recent studies in Drosophila also highlight a role for ALK in gut muscle differentiation. Indeed, the Drosophila model offers a future arena for the study of ALK, its ligands and signalling cascades. The discovery of activated fusion forms of the ALK tyrosine kinase in anaplastic large cell lymphoma (ALCL) has dramatically improved our understanding of the pathogenesis of these lymphomas and enhanced the pathological diagnosis of this subtype of non-Hodgkin's lymphoma (NHL). Likewise, the realisation that a high percentage of inflammatory myofibroblastic tumours express activated-ALK fusion proteins has clarified the causation of these mesenchymal neoplasms and provided for their easier discrimination from other mesenchymal-derived inflammatory myofibroblastic tumour (IMT) mimics. Recent reports of ALK expression in a range of carcinoma-derived cell lines together with its apparent role as a receptor for PTN and MK, both of which have been implicated in tumourigenesis, raise the possibility that ALK-mediated signalling could play a role in the development and/or progression of a number of common solid tumours. The therapeutic targeting of ALK may prove to have efficacy in the treatment of many of these neoplasms.

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Molecular mechanisms of G₀/G₁ cell‐cycle arrest and apoptosis induced by terfenadine in human cancer cells

Liu¹,

Wang²,

Chen³

et al. 2003

Molecular Carcinogenesis

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Terfenadine (TF), a highly potent histamine H1 receptor antagonist, has been shown to exert no significant central nervous system side effects in clinically effective doses. In this study, we demonstrated that TF induced significant growth inhibition of human cancer cells, including Hep G2, HT 29, and COLO 205 cells, through induction of G(0)/G(1) phase cell-cycle arrest. The minimal dose of TF induced significant G(0)/G(1) arrest in these cells was 1-3 microM. The protein levels of p53, p21/Cip1, and p27/Kip1 were significantly elevated, whereas the kinase activities of cyclin-dependent kinase 2 (CDK2) and CDK4 were inhibited simultaneously in the TF-treated cells. On the other hand, significant apoptosis, but not G(0)/G(1) arrest, was induced in the HL 60 (p53-null) or Hep 3B (with deleted p53) cells when treated with TF (3-5 microM). To clarify the roles of p21/Cip1 and p27/Kip1 protein expression, which was involved in G(0)/G(1) arrest and apoptosis induced by TF in human cancer cells, antisense oligodeoxynucleotides (ODNs) specific to p21/Cip1 and p27/Kip1 were used, and the expression of the p21/Cip1 and p27/Kip1 were monitored by immunoblotting analysis. Our data demonstrated that the percentage of the apoptotic cells detected by annexin V/PI analysis in the TF-treated group was clearly attenuated by pretreatment with p27/Kip1-specific ODNs. These results indicated that p27/Kip1 (but not p21/Cip1) protein indeed played a critical role in the TF-induced apoptosis. We also demonstrated that the TF-induced G(0)/G(1) cell-cycle arrest effect was not reversed by TF removal, and this growth inhibition lasted for at least 7 d. Importantly, the occurrence of apoptosis and cell growth arrest was not observed in the TF-treated normal human fibroblast, even at a dose as high as 25 microM. Our study showed the molecular mechanisms for TF-induced cell growth inhibition and the occurrence of apoptosis in human cancer cells.

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Comparison of the effects of recombinant adenovirus-mediated expression of wild-type p53 and p27Kip1 on cell cycle and apoptosis in SUDHL-1 cells derived from anaplastic large cell lymphoma

Abstract: Recombinant adenoviruses expressing wild-type p53 (AdWTp53) and p27 Kip1

Cited by 8 publications

References 27 publications

Recombinant adenovirus-mediated cytotoxic gene therapy of lymphoproliferative disorders: is CAR important for the vector to ride?

Recombinant adenovirus-mediated cytotoxic gene therapy of lymphoproliferative disorders: is CAR important for the vector to ride?

Anaplastic lymphoma kinase proteins in growth control and cancer

Molecular mechanisms of G₀/G₁ cell‐cycle arrest and apoptosis induced by terfenadine in human cancer cells

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Comparison of the effects of recombinant adenovirus-mediated expression of wild-type p53 and p27Kip1 on cell cycle and apoptosis in SUDHL-1 cells derived from anaplastic large cell lymphoma

Abstract: Recombinant adenoviruses expressing wild-type p53 (AdWTp53) and p27 Kip1

Cited by 8 publications

References 27 publications

Recombinant adenovirus-mediated cytotoxic gene therapy of lymphoproliferative disorders: is CAR important for the vector to ride?

Recombinant adenovirus-mediated cytotoxic gene therapy of lymphoproliferative disorders: is CAR important for the vector to ride?

Anaplastic lymphoma kinase proteins in growth control and cancer

Molecular mechanisms of G0/G1 cell‐cycle arrest and apoptosis induced by terfenadine in human cancer cells

Contact Info

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Molecular mechanisms of G₀/G₁ cell‐cycle arrest and apoptosis induced by terfenadine in human cancer cells