The NF-κB-inducing Kinase Induces PC12 Cell Differentiation and Prevents Apoptosis

Foehr, Erik D; Bohuslav, Jan; Chen, Lin Feng; DeNoronha, Carlos; Geleziunas, Romas; Lin, Xin; O’Mahony, Alison; Greene, Warner C.

doi:10.1074/jbc.c000507200

Cited by 47 publications

(50 citation statements)

References 43 publications

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“…Whereas NF-kB activation via the p75(NTR) receptor significantly blocked apoptosis, its activation via TrkA induced neurite process formation. Similarly, overexpression of NIK induced PC12 cell differentiation and antagonized cell death via the IKK and MAPK signaling cascades (Foehr et al, 2000a). Consistent with these findings in cultured cells, embryos from IKKa/IKKb double knockout mice show defects in neurulation due to increased apoptosis.…”

Section: Anti-and Proapoptotic Roles For Nf-kb In T Cellssupporting

confidence: 75%

To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis

et al. 2003

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Section: Anti-and Proapoptotic Roles For Nf-kb In T Cellssupporting

confidence: 75%

To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis

et al. 2003

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“…After stimulation, nuclear extracts were prepared as previously described (20). For analysis of B enhancer binding proteins, 2.5 l of the nuclear extracts were incubated with poly(dI-dC) and salmon sperm DNA for 10 min, followed by the addition of [␥-32 P]ATP-labeled consensus B or Oct-1 enhancer oligonucleotides (Promega).…”

Section: Methodsmentioning

confidence: 99%

Prostratin Antagonizes HIV Latency by Activating NF-κB

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Kwon

et al. 2004

Journal of Biological Chemistry

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“…miR-520e inhibits growth of hepatoma cells S Zhang et al (MAP3K14, NM_003954.2) was of particular interest, because it was found to be upstream of NF-kB and correlated with growth of cancer cells, including human prostate cancer, breast cancer and melanotic cancer (Foehr et al, 2000;Dhawan and Richmond, 2002;Nishina et al, 2009;Yamaguchi et al, 2009). As shown in Figure 5a, there was a miR-520e binding site at nt1033-1039 of the NIK 3 0 UTR.…”

Section: Resultsmentioning

confidence: 99%

“…NIK is a member of the mitogenactivated protein kinase kinase kinase family that may either directly or indirectly phosphorylate or activate IKKa/b, leading to the phosphorylation and degradation of IkBa followed by NF-kB activation. Foehr et al, 2000 have recently demonstrated that NIK regulates differentiation of PC-12 cells through MEK/ERK pathways. Rangaswami et al (2004) reported that NIK has a crucial role in OPN-induced NF-kB activation, uPA secretion and pro-MMP-9 activation through MAPK/IKKa/b-mediated pathways, and all of these ultimately control tumor growth.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-520e suppresses growth of hepatoma cells by targeting the NF-κB-inducing kinase (NIK)

et al. 2011

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MicroRNAs (miRNAs) are small, non-coding RNAs that can act as oncogenes or tumor suppressor genes in human cancer. Emerging evidence indicates that deregulation of miRNAs contributes to the hepatocarcinogenesis. In the present study, we demonstrated that the levels of miR-520e were dramatically decreased in examined hepatoma cell lines and clinical hepatocellular carcinoma (HCC) tissues. Moreover, we found that DNA hypermethylation in the upstream region of miR-520e resulted in the downregulation of miR-520e. Next, we demonstrated that introduction of miR-520e dramatically suppressed the growth of hepatoma cells in vitro and in vivo, whereas silencing the expression of miR-520e by anti-miR-520e resulted in a promoted cell proliferation, suggesting that miR-520e may be a novel tumor suppressor. Further studies revealed that NF-jB-inducing kinase (NIK) was one of the direct target genes of miR-520e, as miR-520e directly bound to the 3 0 untranslated region of NIK, which reduced the expression of NIK at the levels of mRNA and protein. Moreover, silencing of NIK was able to inhibit the growth of hepatoma cells, similar to the effect of miR-520e overexpression on growth of hepatoma cells. Meanwhile, the knockdown of NIK expression reversed the enhanced proliferation mediated by anti-miR-520e. In addition, miR-520e significantly decreased the phosphorylation of ERK1/2 (p-ERK1/2) and depressed the transcriptional activity and nuclear translocation of nuclear factor jB (NF-jB) (p65). These results suggest that miR-520e suppresses the growth of hepatoma cells by targeting NIK involving the NIK/p-ERK1/2/NF-jB signaling pathway. Finally, we showed that the intratumoral injection with miR-520e was able to directly repress the growth of hepatoma cells in the nude mice. Thus, our finding provides new insight into the mechanism of hepatocarcinogenesis, indicating a therapeutic potential of miR-520e in the treatment of HCC.

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The NF-κB-inducing Kinase Induces PC12 Cell Differentiation and Prevents Apoptosis

Abstract: NF-B has been implicated in

Cited by 47 publications

References 43 publications

To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis

To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis

Prostratin Antagonizes HIV Latency by Activating NF-κB

MicroRNA-520e suppresses growth of hepatoma cells by targeting the NF-κB-inducing kinase (NIK)

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