The cytokine CSF-1 (M-CSF) expressed by endometrial carcinomas in vivo and in vitro, may also be a circulating tumor marker of neoplastic disease activity in endometrial carcinoma patients

Kacinski, Barry M.; Chambers, Setsuko K.; Stanley, E. Richard; Carter, Darryl; Tseng, Paul C.; Scata, Kimberly A.; Chang, D.; Pirro, Mary; Nguyen, Josephine T.; Ariza, Aurelio; Rohrschneider, Larry R.; Rothwell, Victoria

doi:10.1016/0360-3016(90)90488-6

Cited by 54 publications

(25 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Here we examine the consequences of activation of the colony stimulating factor-1 receptor (CSF-1R). This receptor tyrosine kinase (RTK) is not expressed in normal nonlactating mammary glands but recent reports by several laboratories indicate that 58 ± 90% of invasive breast tumors may express CSF-1R (Kacinski et al, 1991;Tang et al, 1992;Scholl et al, 1994). An antibody that recognizes tyrosine phosphorylated CSF-1R stained 52% of the invasive tumors, indicating that CSF-1R is activated in breast cancer (Flick et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

CSF-1 activates MAPK-dependent and p53-independent pathways to induce growth arrest of hormone-dependent human breast cancer cells

1999

View full text Add to dashboard Cite

The CSF-1 receptor (CSF-1R) is expressed in 450% of human breast cancers. To investigate the consequence of CSF-1R expression, hormone-dependent human breast cancer cell lines, MCF-7 and T-47D, were transfected with CSF-1R. Unexpectedly, CSF-1 substantially inhibited estradiol (E 2 ) and insulin-dependent proliferation of MCF-7 transfectants (MCF-7fms) and prevented cyclin E/cdk2 and cyclin A/cdk2 activation, consistent with a G 1 arrest. In contrast, CSF-1 increased DNA synthesis in T-47D transfectants (T-47Dfms) alone and with E 2 or insulin. In response to CSF-1, there was a marked and sustained upregulation of the cyclindependent kinase inhibitor, p21, in MCF-7fms but not T-47Dfms. CSF-1 also markedly upregulated cyclin D1 in MCF-7fms. The coordinate increase in cyclin D1 and p21 had the eect of decreasing the speci®c but not absolute activity of cyclin D1/cdk4. p53 was not involved since CSF-1 induction of p21 was unaected by dominant-negative p53 expression. ERK activation by CSF-1 was robust and sustained in MCF7fms and to a much lesser extent in T-47Dfms. Using pharmacological and transient transfection approaches, we showed that ERK activation was necessary and sucient for p21 induction in MCF-7fms. Moreover, activated MEK inhibited E 2 -stimulated cdk2 activity. Our ®ndings indicate that the consequence of CSF-1R-mediated signals in human breast cancer cells is dependent on the genetic background of the particular tumor.

show abstract

Section: Introductionmentioning

confidence: 99%

CSF-1 activates MAPK-dependent and p53-independent pathways to induce growth arrest of hormone-dependent human breast cancer cells

1999

View full text Add to dashboard Cite

show abstract

“…Isolation of protein fractions responsible for this activity resulted in the recognition that several families of growth factors, including epidermal growth factor (EGF), transforming growth factor a (TGFa), ®broblast growth factor (FGF), insulin and insulin-like growth factors (IGF's) were important in the growth of these cells. Likewise cell-surface receptors for these growth factors have been identi®ed on breast cells and are found with variable frequency in primary human breast tumor samples (Dickson and Lippman, 1992;Kacinski et al, 1991;Harris, 1994;Chrysagekos and Dickson, 1994). Despite these observations, reproducible growth of primary breast cancer cells in vitro remains di cult (Ethier et al, 1993;Petersen et al, 1992;Stampfer and Yaswen, 1993).…”

Section: Introductionmentioning

confidence: 99%

Expression and function of members of the cytokine receptor superfamily on breast cancer cells

et al. 1997

View full text Add to dashboard Cite

“…In cancer, the elevated expression of CSF1R in malignant epithelial cells of breast, ovary, pancreas and lung carcinomas correlates with high tumor grade and poor prognosis (Kacinski et al, 1988(Kacinski et al, , 1989(Kacinski et al, , 1990Tang et al, 1992;Scholl et al, 1994).…”

mentioning

confidence: 99%

A novel function of colony-stimulating factor 1 receptor in hTERT immortalization of human epithelial cells

Kocher

Salako

et al. 2008

Oncogene

View full text Add to dashboard Cite

The receptor for macrophage colony-stimulating factor 1 receptor (CSF1R) is a product of the proto-oncogene c-fms and a member of the class III transmembrane tyrosine kinase receptor family. Earlier, we described increased mRNA expression of CSF1R in human telomerase reverse transcriptase (hTERT) immortalized human ovarian surface epithelial (IOSE) cell lines derived from a single donor. Here, we further describe that CSF1R is upregulated at both the mRNA and protein level in hTERT immortalized human normal OSE cells from two different donors and in hTERT immortalized human pancreatic ductal epithelial cells. CSF1R was not upregulated in hTERT immortalized epithelial clones that subsequently underwent senescence or in immortalized fibroblasts. Upon stimulation by the CSF1R ligand CSF1, the immortalized epithelial cell lines showed rapid internalization of CSF1R with concomitant down-modulation and colocalization of phosphorylated NFjBp65 with hTERT protein, hTERT translocation into the nucleus and the binding of c-Myc to the hTERT promoter region. Reducing the expression of CSF1R using short hairpin interfering RNA abolished these effects and also decreased cell survival and the number of population doublings under suboptimal culture conditions. The telomerase inhibitor GRN163L confirmed a role for telomerase in the cleavage of the intracellular domain of CSF1R. On the basis of these findings, we suggest that CSF1R may be a critical factor facilitating hTERT immortalization of epithelial cells.

show abstract

The cytokine CSF-1 (M-CSF) expressed by endometrial carcinomas in vivo and in vitro, may also be a circulating tumor marker of neoplastic disease activity in endometrial carcinoma patients

Cited by 54 publications

References 13 publications

CSF-1 activates MAPK-dependent and p53-independent pathways to induce growth arrest of hormone-dependent human breast cancer cells

CSF-1 activates MAPK-dependent and p53-independent pathways to induce growth arrest of hormone-dependent human breast cancer cells

Expression and function of members of the cytokine receptor superfamily on breast cancer cells

A novel function of colony-stimulating factor 1 receptor in hTERT immortalization of human epithelial cells

Contact Info

Product

Resources

About