Downregulation of Mdm2 and Mdm4 enhances viral gene expression during adenovirus infection

Yang, Heng; Zheng, Zhi-Ming; Zhao, Lisa; Li, Qiang

doi:10.4161/cc.11.3.19052

Cited by 13 publications

(13 citation statements)

References 71 publications

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“…Viability was assayed at 24 h and 48 h post infection. For Western blotting, cells in multiple-well plates were lysed and processed as described previously57. Antibodies used for Western blotting detection included those against Ad12 E1A, Ad5 DBP (B6–8), and Ad5 capsids as previously described57.…”

Section: Methodsmentioning

confidence: 99%

“…For Western blotting, cells in multiple-well plates were lysed and processed as described previously57. Antibodies used for Western blotting detection included those against Ad12 E1A, Ad5 DBP (B6–8), and Ad5 capsids as previously described57. In addition, an custom-made anti-Ad12 E1A polyclonal antibody by YenZym Antibodies, LLC was also used for detecting Ad12 E1A.…”

Section: Methodsmentioning

confidence: 99%

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Intrinsic cellular signaling mechanisms determine the sensitivity of cancer cells to virus-induced apoptosis

Wang

Luo

et al. 2016

Sci Rep

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Cancer cells of epithelial and mesenchymal phenotypes exhibit different sensitivities to apoptosis stimuli, but the mechanisms underlying this phenomenon remain partly understood. We constructed a novel recombinant adenovirus expressing Ad12 E1A (Ad-E1A12) that can strongly induce apoptosis. Ad-E1A12 infection of epithelial cancer cells displayed dramatic detachment and apoptosis, whereas cancer cells of mesenchymal phenotypes with metastatic propensity were markedly more resistant to this virus. Notably, forced detachment of epithelial cells did not further sensitize them to Ad-E1A12-induced apoptosis, suggesting that cell detachment is a consequence rather than the cause of Ad-E1A12-induced apoptosis. Ad-E1A12 increased phosphorylation of AKT1 and ribosomal protein S6 through independent mechanisms in different cell types. Ad-E1A12–induced AKT1 phosphorylation was PI3K-dependent in epithelial cancer cells, and mTOR-dependent in mesenchymal cancer cells. Epithelial cancer cells upon Ad-E1A12-induced detachment could not sustain AKT activation due to AKT1 degradation, but AKT1 activation was maintained in mesenchymal cancer cells. Expression of epithelial cell-restricted miR-200 family in mesenchymal cells limited mTOR signaling and sensitized them to Ad-E1A12-induced cell killing. Thus, epithelial cancer cells rely on the canonical PI3K-AKT signaling pathway for survival, while mesenchymal cancer cells deploy the PI3K-independent mTORC2-AKT axis in response to strong death stimuli.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Intrinsic cellular signaling mechanisms determine the sensitivity of cancer cells to virus-induced apoptosis

Wang

Luo

et al. 2016

Sci Rep

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“…Anti‐GFP mouse monoclonal antibody was from Babco (BioLegend, San Diego, CA). Anti‐adenovirus type 5 DNA‐binding protein (DBP) antibody (B6‐8) was as described previously …”

Section: Methodsmentioning

confidence: 99%

Inhibition of androgen receptor transactivation function by adenovirus type 12 E1A undermines prostate cancer cell survival

Tian

Wang

et al. 2018

The Prostate

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“…Loss of p53 confers enhanced susceptibility to reoviral and myxoma infectivity and replication (45). The role of p53 status appears to be even more essential for the replication of viruses that are implicated in tumorigenesis: human papillomaviruses (46–48), hepatitis B virus (49–52), gallid herpesvirus 2, which causes T-cell lymphomas in chickens (53), human adenoviruses (54, 55), and HSV-1 (56). …”

Section: Introductionmentioning

confidence: 99%

The p53–microRNA-34a axis regulates cellular entry receptors for tumor-associated human herpes viruses

et al. 2013

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A growing number of reports indicate the frequent presence of DNA sequences and gene products of human cytomegalovirus in various tumors as compared to adjacent normal tissues, the brain tumors being studied most intensely. The mechanisms underlying the tropism of human cytomegalovirus to the tumor cells or to the cells of tumor origin, as well as the role of the host’s genetic background in virus-associated oncogenesis are not well understood. It is also not clear why cytomegalovirus can be detected in many but not in all tumor specimens. Our in silico prediction results indicate that microRNA-34a may be involved in replication of some human DNA viruses by targeting and downregulating the genes encoding a diverse group of proteins, such as platelet-derived growth factor receptor-alpha, complement component receptor 2, herpes simplex virus entry mediators A, B, and C, and CD46. Notably, while their functions vary, these surface molecules have one feature in common: they serve as cellular entry receptors for human DNA viruses (cytomegalovirus, Epstein-Barr virus, human herpes virus 6, herpes simplex viruses 1 and 2, and adenoviruses) that are either proven or suspected to be linked with malignancies. MicroRNA-34a is strictly dependent on its transcriptional activator tumor suppressor protein p53, and both p53 and microRNA-34a are frequently mutated or downregulated in various cancers. We hypothesize that p53 – microRNA-34a axis may alter susceptibility of cells to infection with some viruses that are detected in tumors and either proven or suspected to be associated with tumor initiation and progression.

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Downregulation of Mdm2 and Mdm4 enhances viral gene expression during adenovirus infection

Cited by 13 publications

References 71 publications

Intrinsic cellular signaling mechanisms determine the sensitivity of cancer cells to virus-induced apoptosis

Intrinsic cellular signaling mechanisms determine the sensitivity of cancer cells to virus-induced apoptosis

Inhibition of androgen receptor transactivation function by adenovirus type 12 E1A undermines prostate cancer cell survival

The p53–microRNA-34a axis regulates cellular entry receptors for tumor-associated human herpes viruses

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