Varying sensitivity of human mammary carcinoma cells to the toxic effect of parvovirus H-1

Pachterbeke, C. Van; Tuynder, Marcel; Brandenburger, Anne-Nicole; Leclercq, Guy; Borrás, M.; Rommelaere, Jean

doi:10.1016/s0959-8049(97)00153-6

Cited by 19 publications

(18 citation statements)

References 13 publications

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“…PV H-1PV efficiently suppresses these MYC-dependent tumors in preclinical models (refs. 50,51;Lacroix,unpublished data). In response to PV infection, MYC expression is repressed in various cancer cell lines of different origins (refs.…”

Section: Implications For Cancer Parvovirotherapymentioning

confidence: 91%

Molecular Pathways: Rodent Parvoviruses—Mechanisms of Oncolysis and Prospects for Clinical Cancer Treatment

Nüesch

Lacroix

Marchini

et al. 2012

Clinical Cancer Research

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Rodent parvoviruses (PV) are recognized for their intrinsic oncotropism and oncolytic activity, which contribute to their natural oncosuppressive effects. Although PV uptake occurs in most host cells, some of the subsequent steps leading to expression and amplification of the viral genome and production of progeny particles are upregulated in malignantly transformed cells. By usurping cellular processes such as DNA replication, DNA damage response, and gene expression, and/or by interfering with cellular signaling cascades involved in cytoskeleton dynamics, vesicular integrity, cell survival, and death, PVs can induce cytostasis and cytotoxicity. Although productive PV infections normally culminate in cytolysis, virus spread to neighboring cells and secondary rounds of infection, even abortive infection or the sole expression of the PV nonstructural protein NS1, is sufficient to cause significant tumor cell death, either directly or indirectly (through activation of host immune responses). This review highlights the molecular pathways involved in tumor cell targeting by PVs and in PV-induced cell death. It concludes with a discussion of the relevance of these pathways to the application of PVs in cancer therapy, linking basic knowledge of PV-host cell interactions to preclinical assessment of PV oncosuppression. Clin Cancer Res; 18(13); 3516-23. Ó2012 AACR.

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Section: Implications For Cancer Parvovirotherapymentioning

confidence: 91%

Molecular Pathways: Rodent Parvoviruses—Mechanisms of Oncolysis and Prospects for Clinical Cancer Treatment

Nüesch

Lacroix

Marchini

et al. 2012

Clinical Cancer Research

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“…The inherent oncotropism of these autonomous parvoviruses is based on their dependence on cellular proliferation factors expressed during the S phase and the differentiated state of the host cell (6,7). The rodent parvoviruses display oncopreferential cytotoxic activity in vitro and also possess an oncosuppressive potential, inhibiting the formation of spontaneous and chemical or virus-induced tumors in vitro and in vivo (8)(9)(10)(11)(12)(13). These viruses can also persistently infect their natural hosts, do not integrate their genome into cellular chromosomes, and are not associated with human disease (reviewed in reference 4).…”

Section: H -1 Parvovirus (H-1pvmentioning

confidence: 99%

Structural Characterization of H-1 Parvovirus: Comparison of Infectious Virions to Empty Capsids

Halder

Nam

Govindasamy

et al. 2013

J Virol

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bThe structure of single-stranded DNA (ssDNA) packaging H-1 parvovirus (H-1PV), which is being developed as an antitumor gene delivery vector, has been determined for wild-type (wt) virions and noninfectious (empty) capsids to 2.7-and 3.2-Å resolution, respectively, using X-ray crystallography. The capsid viral protein (VP) structure consists of an ␣-helix and an eightstranded anti-parallel ␤-barrel with large loop regions between the strands. The ␤-barrel and loops form the capsid core and surface, respectively. In the wt structure, 600 nucleotides are ordered in an interior DNA binding pocket of the capsid. This accounts for ϳ12% of the H-1PV genome. The wt structure is identical to the empty capsid structure, except for side chain conformation variations at the nucleotide binding pocket. Comparison of the H-1PV nucleotides to those observed in canine parvovirus and minute virus of mice, two members of the genus Parvovirus, showed both similarity in structure and analogous interactions. This observation suggests a functional role, such as in capsid stability and/or ssDNA genome recognition for encapsulation. The VP structure differs from those of other parvoviruses in surface loop regions that control receptor binding, tissue tropism, pathogenicity, and antibody recognition, including VP sequences reported to determine tumor cell tropism for oncotropic rodent parvoviruses. These structures of H-1PV provide insight into structural features that dictate capsid stabilization following genome packaging and three-dimensional information applicable for rational design of tumor-targeted recombinant gene delivery vectors. H -1 parvovirus (H-1PV) is a member of the rodent subgroup of the Parvovirus genus of the single-stranded DNA (ssDNA) Parvoviridae (1). H-1PV was first isolated from rats transplanted with HEP-1, a human liver adenocarcinoma cell line (2), and also from aborted human fetuses (3). Recombinant vectors based on H-1PV and a number of other rodent parvoviruses, including minute virus of mice (MVM) and LuIII, are promising candidates for antitumor delivery vectors, particularly for cytoreductive and immunogene therapy approaches (reviewed in references 4 and 5). The inherent oncotropism of these autonomous parvoviruses is based on their dependence on cellular proliferation factors expressed during the S phase and the differentiated state of the host cell (6, 7). The rodent parvoviruses display oncopreferential cytotoxic activity in vitro and also possess an oncosuppressive potential, inhibiting the formation of spontaneous and chemical or virus-induced tumors in vitro and in vivo (8-13). These viruses can also persistently infect their natural hosts, do not integrate their genome into cellular chromosomes, and are not associated with human disease (reviewed in reference 4).Recombinant rodent parvovirus vectors targeted for tumor therapy utilize a double-edged strategy that takes advantage of their inherent oncotropism and selective cytotoxicity plus their ability to deliver therapeutic genes that code for ...

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“…svitlana Grekova, 1, * Marc aprahamian, 1 Nathalia Giese, 2 steffen schmitt, 3 Thomas Giese, 4 Christine s. Falk, 5 Laurent Daeffler, offers improvement of long-term survival, but it is feasible in only a minority of patients and is not without risk. 8 To downstage a tumor towards operability, neoadjuvant approaches combining radio-, chemo-and immuno-therapeutic modalities are increasingly gaining acceptance.…”

Section: Immune Cells Participate In the Oncosuppressive Activity Of mentioning

confidence: 99%

“…Over the last few decades, the molecular bases of PV oncotropism and oncolytic activity have been extensively studied for different types of malignancies both in vitro and in preclinical models. [4][5][6][7] Despite undisputable progress in cancer diagnosis and therapy during the 20 th century and the improved prognosis of several types of tumors, pancreatic ductal adenocarcinoma (PDAC) still remains one of the malignancies with the worst survival rates. The disease is highly resistant to current treatments.…”

Section: Introductionmentioning

confidence: 99%

Immune cells participate in the oncosuppressive activity of parvovirus H-1PV and are activated as a result of their abortive infection with this agent

Grekova¹,

Aprahamian²,

Giese³

et al. 2010

Cancer Biology & Therapy

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Varying sensitivity of human mammary carcinoma cells to the toxic effect of parvovirus H-1

Cited by 19 publications

References 13 publications

Molecular Pathways: Rodent Parvoviruses—Mechanisms of Oncolysis and Prospects for Clinical Cancer Treatment

Molecular Pathways: Rodent Parvoviruses—Mechanisms of Oncolysis and Prospects for Clinical Cancer Treatment

Structural Characterization of H-1 Parvovirus: Comparison of Infectious Virions to Empty Capsids

Immune cells participate in the oncosuppressive activity of parvovirus H-1PV and are activated as a result of their abortive infection with this agent

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