Derangement of growth and differentiation control in oncogenesis

Corn, Paul G.; El‐Deiry, Wafik S.

doi:10.1002/bies.10036

Cited by 29 publications

(24 citation statements)

References 51 publications

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“…Tumor transformation involves the progressive accumulation of genetic and epigenetic alterations to tumor suppressor genes and oncogenes (Ross et al, 2000;Corn and El-Deiry, 2002). The genes that are altered during tumorigenesis mainly affect cell growth, apoptosis, and the differentiation of tumor cells.…”

Section: Introductionmentioning

confidence: 99%

VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D3 inhibits tumor cell growth by blocking cell-cycle progression

Han¹,

Jeon²,

Ju³

et al. 2003

Oncogene

258

235

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Vitamin D 3 upregulated protein 1 (VDUP1) is a 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ) upregulated protein, and it is induced by various stresses. In human tumor tissues, VDUP1 expression was downregulated. Upon stimulation by growth-inhibitory signals such as TGF-b1 and 1,25(OH) 2 D 3 , its expression was rapidly upregulated as the cell growth was retarded. The transfection of VDUP1 in tumor cells reduced cell growth. The VDUP1 expression was also increased when the cell-cycle progression was arrested. Transfection of VDUP1 induced cellcycle arrest at the G0/G1 phase, indicating that VDUP1 possesses a tumor-suppressive activity. In addition, it was found that VDUP1 interacted with promyelocytic leukemia zinc-finger, Fanconi anemia zinc-finger, and histone deacetylase 1, which are known to be transcriptional corepressors. VDUP1 itself suppressed IL-3 receptor and cyclin A2 promoter activity. Taken together, these results suggest that VDUP1 is a novel antitumor gene which forms a transcriptional repressor complex.

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Section: Introductionmentioning

confidence: 99%

VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D3 inhibits tumor cell growth by blocking cell-cycle progression

Han¹,

Jeon²,

Ju³

et al. 2003

Oncogene

258

235

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show abstract

“…Meticulously regulated differentiation, proliferation and apoptosis play fundamental roles in the development of multicellular organisms and the maintenance of tissue homeostasis (Abrams 2002, Corn & El-Deiry 2002. We previously found that ACTH is able to induce differentiation and apoptosis, but it inhibits proliferation of rat fetal adrenocortical cells in primary cultures (Arola et al 1993).…”

Section: Introductionmentioning

confidence: 99%

cAMP-dependent protein kinase activation inhibits proliferation and enhances apoptotic effect of tumor necrosis factor-α in NCI-H295R adrenocortical cells

Liu

Ora

et al. 2004

Journal of Molecular Endocrinology

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Adrenocorticotropin is the major regulator of adrenocortical development and function. It acts mainly through the cAMP-dependent protein kinase A (PKA) pathway. Our aim was to study the interaction of tumor necrosis factor-(TNF ) and the PKA pathway in adrenocortical cell proliferation and apoptosis. The PKA activator Dibutyryl cAMP ((Bu) 2 cAMP) strongly induced differentiation and inhibited proliferation in the human adrenocortical cell line NCI-H295R (H295R). TNF induced apoptosis of H295R cells. Interestingly, (Bu) 2 cAMP treatment clearly enhanced TNF -induced apoptosis in H295R cells, but not in another human adrenocortical cell line SW-13, the mouse adrenocortical Y-1 cell line or the human HeLa cell line. This synergistic effect was not due to the (Bu) 2 cAMP-induced glucocorticoid secretion since dexamethasone had no significant effect on the TNF -induced apoptosis. (Bu) 2 cAMP treatment rapidly increased the expression of the proto-oncogene c-myc in H295R cells, but not in SW-13, Y-1 or HeLa cells. In transient c-myc transfection assay, c-myc expression associated with decreased expression of the proliferation marker Ki-67 in H295R cells. In conclusion, cAMP-dependent protein kinase activation reduced proliferation and augmented TNF -induced apoptosis in adrenocortical H295R cells, and these effects were associated with increased c-myc expression.

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“…Liver stem cells proliferate, then differentiate, in response to trauma, stress, or during normal development [22]. HepG2 cells recapitulate this balance, as they are capable of both proliferation and differentiation.…”

Section: Discussionmentioning

confidence: 96%

Effects of Retinoic Acid on Proliferation and Differentiation of HepG2 Cells

Burley¹,

Roth²

2007

TOBIOTJ

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Hepatoma cell lines have characteristics derived from both their hepatic lineage and their transformation. We examined the potential of retinoic acid to enhance the function of a hepatoma cell line, HepG2, under conditions of reduced serum as are desired for bioreactor cultivation. We found that retinoic acid drastically slows the growth of HepG2 cells and induces a more spread morphology. Retinoic acid also augments the differentiated function of the cells, as measured by albumin and urea secretion rates. Expression levels of a panel of liver-enriched transcription factor were increased from retinoic acid exposure. Overall, we demonstrate that retinoic acid has significant effects on HepG2 growth and differentiated function. These results have implications for the use of retinoic acid both as a chemotherapeutic agent and as a medium component for cells of hepatic origin.

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Derangement of growth and differentiation control in oncogenesis

Cited by 29 publications

References 51 publications

VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D3 inhibits tumor cell growth by blocking cell-cycle progression

VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D3 inhibits tumor cell growth by blocking cell-cycle progression

cAMP-dependent protein kinase activation inhibits proliferation and enhances apoptotic effect of tumor necrosis factor-α in NCI-H295R adrenocortical cells

Effects of Retinoic Acid on Proliferation and Differentiation of HepG2 Cells

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