Insulin-like Growth Factor I Secreted from Prostate Stromal Cells Mediates Tumor-Stromal Cell Interactions of Prostate Cancer

Kawada, Manabu; Inoue, Hiroyuki; Masuda, Tohru; Ikeda, Daishiro

doi:10.1158/0008-5472.can-05-4239

Cited by 74 publications

(84 citation statements)

References 41 publications

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“…5 In the coculture, the growth of DU-145 cells is increased by PrSC. 3,5 As shown in Figure 4, all compounds showed selective growth inhibitory activities and inhibited the growth of DU-145 cells in coculture with PrSC more strongly than that of DU-145 cells alone. The IC 50 values of 1-5 against the growth of DU-145 cells in coculture were 0.21, 0.021, 0.034, 0.064 and 0.13 mg ml À1 , respectively, whereas those of 1-5 against the growth of DU-145 cells alone were 0.85, 0.048, 0.54, 0.95 and 0.71 mg ml À1 , respectively.…”

Section: Biological Activitiesmentioning

confidence: 94%

“…1,2 We have reported earlier that prostate stromal cell (PrSC) promotes the growth of human prostate cancer cells through the secretion of insulin-like growth factor-I. 3,4 There is a possibility that small molecules could inhibit cancer cell growth by modulating tumor-stromal cell interactions. We developed the in vitro coculture system of human prostate cancer cells and PrSC, in which the growth of prostate cancer cell is increased by the coculture with PrSC.…”

Section: Introductionmentioning

confidence: 99%

“…We developed the in vitro coculture system of human prostate cancer cells and PrSC, in which the growth of prostate cancer cell is increased by the coculture with PrSC. 3,5 Using the assay method, we have been searching for the modulators of the tumor-stromal cell interactions. In the course of our screening of the modulators, we isolated new atpenins, NBRI23477 A (4) and B (5), along with the known compounds, atpenin A4 (1), A5 (2) and B (3).…”

Section: Introductionmentioning

confidence: 99%

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New atpenins, NBRI23477 A and B, inhibit the growth of human prostate cancer cells

et al. 2009

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The growth and metastasis of prostate cancer are regulated by prostate stroma through the tumor-stromal cell interactions. Small molecules that modulate the tumor-stromal cell interactions will be new anticancer drugs. In the course of our screening of the modulators, we isolated two new atpenins, NBRI23477 A (4) and B (5), from the fermentation broth of Penicillium atramentosum PF1420. Compounds 4 and 5 as well as atpenin A4 (1), A5 (2) and B (3) inhibited the growth of human prostate cancer DU-145 cells in the coculture with human prostate stromal cells more strongly than that of DU-145 cells alone.

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Section: Biological Activitiesmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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New atpenins, NBRI23477 A and B, inhibit the growth of human prostate cancer cells

et al. 2009

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“…51 Stromal IGF-1 mediates tumour-stromal interactions in PCa to accelerate tumour growth. 52 PCa epithelia are sensitive to surrounding IGF-1 levels, regardless of their androgen sensitivity status. 18 Androgen treatment had opposing effects on IGF-1 secretion from the two stromal cell types, namely, it boosted IGF-1 secretion from PZsc but inhibited IGF-1 secretion from TZsc.…”

Section: Differential Effects Of Pzsc and Tzsc On Pc3 Cellsmentioning

confidence: 99%

The differential effects of prostate stromal cells derived from different zones on prostate cancer epithelial cells under the action of sex hormones

Jiang

Han²,

Zhao³

et al. 2011

Asian J Androl

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It is well known that prostate cancer (PCa) occurs predominantly in the peripheral zone (PZ), whereas benign prostatic hyperplasia (BPH) typically develops in the transition zone. To identify possible mechanisms underlying zonal differences, we compared the effects of prostate stromal cells derived from the peripheral zone (PZsc) and the transition zone (TZsc) on a PCa epithelial cell line (PC3) in the presence of sex hormones. First, we observed that androgen receptor (AR) mRNA was more highly expressed in PZsc than TZsc when the cells were treated with dihydrotestosterone (DHT) and b-oestradiol (E2) (P,0.05). By ELISA, we looked for differences in the secretion of peptide growth factors from PZsc and TZsc. We found that keratinocyte growth factor (KGF) secretion increased with increasing concentrations of DHT (P,0.01) and was higher in PZsc than TZsc. Under treatment with DHT plus E2, PZsc secreted more transforming growth factor-b1 (TGF-b1) than TZsc, but this pattern was reversed when the cells were treated with E2 only. With increasing concentrations of DHT, insulin-like growth factor-1 (IGF-1) secretion increased in PZsc but decreased in TZsc. To further characterize the effects of PZsc and TZsc on PC3 cells, we developed a coculture model and performed MTT assays, Western blot analysis and real-time RT-PCR. We found that PZsc promoted PC3 cell proliferation and progression better than TZsc, particularly when treated with 10 nmol l 21 DHT plus 10 nmol l 21 E2. In conclusion, our data suggest that PZsc may have a greater capacity to induce PCa development and progression than TZsc via growth factors regulated by sex hormones. These findings provide possible mechanisms underlying zonal differences in prostate diseases, which may aid the search for novel therapeutic targets for PCa.

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“…These include the following: fibroblast growth factor, insulin-like growth factor (IGF), epithelial growth factor, hepatocyte growth factor, and transforming growth factor-␤. Although most of these factors are predominantly stimulators of proliferation, [11][12][13][14][15][16] some can have dual functions as both stimulators of proliferation and promoters of cell death. 17,18 Differential expression of some genes in the stroma has been shown to produce signals that affect epithelial cell growth.…”

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confidence: 99%

Stromally Expressed c-Jun Regulates Proliferation of Prostate Epithelial Cells

Febbo

et al. 2007

The American Journal of Pathology

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Stromal-epithelial interactions play a critical role inBenign prostatic hyperplasia (BPH) is the most common age-related proliferative abnormality of the human prostate affecting elderly men throughout the world. Half of all men have BPH identifiable histologically by age 60, and by age 85 the prevalence is ϳ90%. 1 The excessive cell proliferation associated with BPH causes benign prostatic enlargement, bladder outlet obstruction, and lower urinary tract symptoms, which afflict the patients. 2 BPH is a histological diagnosis associated with both epithelial and stromal (fibroblasts and smooth muscle cells of prostate) hyperplasia. 3 Cellular alterations that include changes in proliferation, differentiation, apoptosis, and senescence in the epithelium and stroma are implicated in the pathogenesis of BPH. Medical treatments available to patients with BPH target both prostatic stromal and epithelial cells.Watchful waiting, pharmacological therapy, and surgery are three treatment modalities for BPH patients. Medical therapy is a long-term commitment for the patient. Surveys show that a large number of patients discontinue therapy, often because they perceive lack of efficacy and/or experience side effects. 4,5 We can accordingly improve our treatment of BPH by better targeted medical therapy to decrease the number of invasive therapies for this benign disease. Better alternative and improved therapies can be achieved by studying the normal and abnormal reciprocal cross talk between prostatic stromal and epithelial cells.Stromal-epithelial interactions play a critical role in the development and growth of the prostate gland and BPH. Cunha and colleagues 6 -8 have demonstrated that the stromal embryonic tissue is responsible for instructing the proper development of prostate epithelial cells. Tissue recombinants between embryonic urogenital sinus mesenchyme and adult prostatic tissue have demonstrated that the fetal mesenchyme can drive differentiation and growth of adult prostatic epithelial cells. 9 It has been proposed that BPH may be caused by reactivation of dormant embryonic growth in the adult stroma. 10 The proliferation of the stromal elements can stimulate the ingrowth of epithelial cells to produce a benign hyperplastic growth that is recognized

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Insulin-like Growth Factor I Secreted from Prostate Stromal Cells Mediates Tumor-Stromal Cell Interactions of Prostate Cancer

Abstract: Prostate cancer shows high expression of type I insulin-like growth factor (IGF-I) receptor (IGF-IR) and prostate stromal cells (PrSC) produce IGF-I. Although high plasma level of IGF

Cited by 74 publications

References 41 publications

New atpenins, NBRI23477 A and B, inhibit the growth of human prostate cancer cells

New atpenins, NBRI23477 A and B, inhibit the growth of human prostate cancer cells

The differential effects of prostate stromal cells derived from different zones on prostate cancer epithelial cells under the action of sex hormones

Stromally Expressed c-Jun Regulates Proliferation of Prostate Epithelial Cells

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