Neoplastic hepatocyte growth associated with cyclin D1 redistribution from the cytoplasm to the nucleus in mouse hepatocarcinogenesis

Yamamoto, Masahiro; Tamakawa, Susumu; Yoshie, Masumi; Yaginuma, Yuji; Ogawa, Katsuhiro

doi:10.1002/mc.20204

Cited by 45 publications

(34 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…SSeCKS was reported to have the capacity to bind to cyclin D1 in quiescent NIH3T3 cells, whereas this binding was disrupted in proliferating cells (Lin et al 2000;Lin and Gelman 2002). In the TNF-a-treated SCs, while proliferation had been suppressed, the binding ability of cyclin D1 with SSeCKS was higher than that in the proliferating SCs, which was similar to that of hepatocellular carcinomas cell (Yamamoto et al 2006). The SSeCKS gene encodes two potential cyclin-binding motifs (CY) flanking major in vivo PKC phosphorylation sites (Ser507/515).…”

Section: Discussionmentioning

confidence: 70%

Tumor necrosis factor‐alpha inhibits Schwann cell proliferation by up‐regulating Src‐suppressed protein kinase C substrate expression

Tao

Cheng

et al. 2009

Journal of Neurochemistry

View full text Add to dashboard Cite

Src‐suppressed protein kinase C substrate (SSeCKS) is a protein kinase C substrate protein, which plays an important role in mitogenic regulatory activity. In the early stage of nerve injury, expression of SSeCKS in the PNS increases, mainly in Schwann cells (SCs). However, the exact function of SSeCKS in the regulation of SC proliferation remains unclear. In this study, we found that tumor necrosis factor‐alpha (TNF‐α) induced both SSeCKS α isoform expression and SC growth arrest in a dose‐dependent manner. By knocking down SSeCKS α isoform expression, TNF‐α‐induced growth arrest in SCs was partially rescued. Concurrently, the expression of cyclin D1 was reduced and the activity of extracellular signal‐regulated kinase 1/2 was decreased. A luciferase activity assay showed that cyclin D1 expression was regulated by SSeCKS at the transcription level. In addition, the cell fragments assay and immunofluorescence revealed that TNF‐α prevented the translocation of cyclin D1 into the nucleus, while knocking down SSeCKS α isoform expression prompted cyclin D1 redistribution to the nucleus. In summary, our data indicate that SSeCKS may play a critical role in TNF‐α‐induced SC growth arrest through inhibition of cyclin D1 expression thus preventing its nuclear translocation.

show abstract

Section: Discussionmentioning

confidence: 70%

Tumor necrosis factor‐alpha inhibits Schwann cell proliferation by up‐regulating Src‐suppressed protein kinase C substrate expression

Tao

Cheng

et al. 2009

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…Cyclin D1 is important for the development and progression of several cancers including those of the breast, oesophagus, bladder and lung [10-19]. Overexpression of cyclin D1 has also been linked to the development of endocrine resistance in breast cancer cells [20-22].…”

Section: Introductionmentioning

confidence: 99%

The regulation of cyclin D1 degradation: roles in cancer development and the potential for therapeutic invention

2007

View full text Add to dashboard Cite

Cyclin D1 is an important regulator of cell cycle progression and can function as a transcriptionl co-regulator. The overexpression of cyclin D1 has been linked to the development and progression of cancer. Deregulated cyclin D1 degradation appears to be responsible for the increased levels of cyclin D1 in several cancers. Recent findings have identified novel mechanisms involved in the regulation of cyclin D1 stability. A number of therapeutic agents have been shown to induce cyclin D1 degradation. The therapeutic ablation of cyclin D1 may be useful for the prevention and treatment of cancer. In this review, current knowledge on the regulation of cyclin D1 degradation is discussed. Novel insights into cyclin D1 degradation are also discussed in the context of ablative therapy. A number of unresolved questions regarding the regulation of cellular cyclin D1 levels are also addressed.

show abstract

“…Cyclin D1 belongs to the highly conserved cyclin family, members of which are characterized by a sequential expression throughout the cell cycle. Mutations, amplification and overexpression of the cyclin D1 gene,CCND1, are observed in a variety of tumors and may contribute to tumorigenesis (Gillett et al, 1996;Hall and Peters, 1996;Yamamoto et al, 2006;Molenaar et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

The zinc-finger protein KCMF1 is overexpressed during pancreatic cancer development and downregulation of KCMF1 inhibits pancreatic cancer development in mice

et al. 2010

View full text Add to dashboard Cite

Potassium channel modulatory factor 1 (KCMF1) was found upregulated in a differential screen in the metaplastic epithelium in the pancreas of transforming growth factor (TGF)-a transgenic mice. Expression analysis indicated broad overexpression in human cancer tissues. Therefore, we investigated the hypothesis that KCMF1 promotes metaplastic changes and tumor development. KCMF1 represents an evolutionarily highly conserved protein with a 95% identity between human and zebrafish. KCMF1 is expressed during embryonic development and in the majority of adult tissues investigated. Upregulation of nuclear KCMF1 expression is evident in preneoplastic lesions and in several epithelial malignancies, such as pancreatic cancer in mice and humans. In cell culture and in the chicken chorioallantoic membrane model, KCMF1 enhances proliferation, migration and invasion of HEK-293 and Panc1 cells. In crossbreeding experiments, KCMF1-knockdown gene trap mice showed a reduced number and size of premalignant lesions and absence of pancreatic cancer formation in TGF-a transgenic mice. This effect is related to the decreased expression of G1 to S cell-cycle regulators such as cyclin D and cyclin-dependent kinase (CDK) 4. Our data support the hypothesis that KCMF1 mediates pro-oncogenic functions in vitro and in vivo and downregulation of KCMF1 results in the inhibition of pancreatic cancer formation in mice. These effects are mediated through downregulation of cell-cycle control genes such as cyclin D and CDK4.

show abstract

Neoplastic hepatocyte growth associated with cyclin D1 redistribution from the cytoplasm to the nucleus in mouse hepatocarcinogenesis

Cited by 45 publications

References 45 publications

Tumor necrosis factor‐alpha inhibits Schwann cell proliferation by up‐regulating Src‐suppressed protein kinase C substrate expression

Tumor necrosis factor‐alpha inhibits Schwann cell proliferation by up‐regulating Src‐suppressed protein kinase C substrate expression

The regulation of cyclin D1 degradation: roles in cancer development and the potential for therapeutic invention

The zinc-finger protein KCMF1 is overexpressed during pancreatic cancer development and downregulation of KCMF1 inhibits pancreatic cancer development in mice

Contact Info

Product

Resources

About