Increased p50/p50 NF-κB Activation in Human Papillomavirus Type 6- or Type 11-Induced Laryngeal Papilloma Tissue

Vancurova, Ivana; Wu, Rongqian; Miskolci, Veronika; Sun, Shishinn

doi:10.1128/jvi.76.3.1533-1536.2002

Cited by 37 publications

(34 citation statements)

References 28 publications

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“…p53-mediated induction of p21 expression may act to protect MCF-7 cells from Cer-induced apoptosis by selectively inducing growth arrest in the G 1 -phase, at least acutely. While p21 has been implicated in mediating p53-dependent apoptosis in response to some chemotherapeutic agents, our findings supported by a body of literature demonstrate that p21 can act as antiapoptotic factor in MCF-7 cells (70,71), as well as other tumor cell lines (20,40,72). This information may be clinically relevant since induction of apoptosis is the preferred treatment response over growth arrest.…”

Section: Discussionsupporting

confidence: 73%

Inhibition of p53 sensitizes MCF-7 cells to ceramide treatment

Struckhoff

Patel²,

Beckman³

2010

Int J Oncol

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Abstract. Ceramide signaling plays an important role in tumor progression and development of chemoresistance, and ceramide-based therapies are proposed as potential therapeutic tools for the treatment of breast cancer. We investigated the effect of exogenous ceramide on the cell cycle progression of MCF-7 breast cancer cells. Ceramide induced a selective arrest of MCF-7 cells in the G 1 -phase, which was associated with a decreased expression of cyclins D and E and increased expression of p53 and p21. Interestingly, inhibition of p53 using pifithrin · or RNAi sensitized MCF-7 cells to ceramide-induced cell death. DNA content analysis suggested that sensitization of cells was due to an increased induction of apoptosis in MCF-7 cells. The increased sensitivity to ceramide, in the context of p53 inhibition, may be due to decreased expression of p21, as siRNA targeted to p21 also sensitized MCF-7 cells to ceramide-induced death. These data demonstrate that in tumors with inactivating mutations of p53, ceramide-based therapies might provide a novel and effective treatment option.

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Section: Discussionsupporting

confidence: 73%

Inhibition of p53 sensitizes MCF-7 cells to ceramide treatment

Struckhoff

Patel²,

Beckman³

2010

Int J Oncol

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“…The formation of NF-kB p50 homodimers, which also act as repressors of NF-kBdependent transcription, and absence of p65 might explain this finding. Recently, a similar pattern of homodimerization of p50 subunits leading to functional inhibition of NF-kB was reported in laryngeal papilloma (37) and cervical (38) and oral carcinoma (39).…”

Section: Discussionmentioning

confidence: 99%

Selective Suppression of NF-kBp65 in Hepatitis Virus-Infected Pregnant Women Manifesting Severe Liver Damage and High Mortality

Prusty

Hedau

Singh

et al. 2007

Mol Med

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Fulminant hepatitis in Asian pregnant women is generally caused by hepatitis E virus infection, and extremely high mortality is most common in them. Decreased cell-mediated immunity is considered a major cause of death in these cases, but what exactly influences decreased immunity and high mortality specifically during pregnancy is not known. We used electrophoretic mobility shift assays, immunoblotting, and immunohistochemical analysis to study the expression and DNA binding activity of NF-kB p50 and NF-kB p65 in pregnant fulminant hepatic failure (FHF) patients and compared them with their nonpregnant counterparts. In both PBMC and postmortem liver biopsy specimens the DNA-binding activity of NF-kB was very high in samples from pregnant FHF patients compared with those from nonpregnant women as well as pregnant women with acute viral hepatitis (AVH) without FHF. Further dissection of the NF-kB complex in supershift assays demonstrated complete absence of p65 in the NF-kB complex, which is formed by homodimerization of the p50 component in pregnant FHF patients. Western blotting and immunohistochemical analysis of the expression of p50 and p65 proteins both showed higher levels of p50 expression and a complete absence or a minimal expression of p65, indicating its nonparticipation in NF-kB-dependent transactivation in pregnant FHF patients. We suggest that the exclusion of p65 from the NF-kB transactivation complex seems to be a crucial step that may cause deregulated immunity and severe liver damage, leading to the death of the patient. Our findings provide a molecular basis, for developing novel therapeutic approaches.

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“…The IκBβ expression was analyzed by two antibodies raised against the C-terminus (C-20) and N-terminus of IκBβ (N-20). Although these antibodies previously identified IκBβ in other human cells (42), no reacting protein was detected in the neutrophils, indicating that human neutrophils do not express the IκBβ protein Figure 1. NFκB activity and cytoplasmic and nuclear levels of IκB and NFκB proteins during persistent neutrophil stimulation with LPS and TNFα.…”

Section: Prolonged Stimulation Of Human Neutrophils With Lps or Tnfα mentioning

confidence: 99%