Role of cyclic AMP and polypeptide growth regulators in growth inhibition by interferon in PC‐3 cells

Okutani, Takuya; Nishi, Nozomu; Kagawa, Yorikazu; Takasuga, Hirotoshi; Takenaka, Ikumasa; Usui, Tsuguru; Wada, Fumio

doi:10.1002/pros.2990180107

Cited by 22 publications

(6 citation statements)

References 19 publications

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“…These observations were confirmed in other investigations (14,(19)(20)(21)23). In the present study, LNCaP cells did not respond to TGF-B, and this observation is in agreement with eariier publications.…”

Section: Discussionsupporting

confidence: 83%

“…Nakamoto and colleagues (31) reported that DU145 and PC-3 cells produced active bFGF and expressed large amounts of bFGF receptors, though only DU145 responded to exogenous bFGF Other studies observed that PC-3 and DU145 cells were insensitive to exogenous bFGF (16,21) and our data support these observations (16,21). The response of LNCaPs to bFGF is variable, with some studies reporting that bFGF stimulates LNCaP growth (32,33).…”

Section: Discussionsupporting

confidence: 81%

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Biological Differences Between Prostate Cancer Cells that Metastasize to Bone Versus Soft Tissue Sites

Pienta¹

2004

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 81%

Biological Differences Between Prostate Cancer Cells that Metastasize to Bone Versus Soft Tissue Sites

Pienta¹

2004

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“…32 It has also been shown that IFN-␣ synergizes with dibutyryl cyclic adenosine 3Ј,5Ј-monophosphate in inducing differentiation in neuroblastoma cells regulating the expression of 2Ј-5Ј-oligoadenylate (2-5A) synthetase at the posttrascriptional level. 33 Both IFN-␣ and 8-Br-cAMP induce intracellular cAMP increase and growth inhibition in a human prostate cancer cell line, 34 and IFN-␥ activates the cAMP/PKA/CREB signaling pathway in murine peritoneal macrophages. 35 Direct involvement of CREB-binding protein/ p300 in sequence-specific DNA binding of type I IFN-dependent transcription factors 36 and the specific interaction between CREB and the transcription factors Stat1 and Stat2 that enhances the transcription of genes regulated by IFN-␣ 37 are well established.…”

Section: Discussionmentioning

confidence: 99%

Adenylate Cyclase/cAMP Pathway Downmodulation Counteracts Apoptosis Induced by IFN-αin Human Epidermoid Cancer Cells

Naviglio

Spina

Marra

et al. 2007

Journal of Interferon & Cytokine Research

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We have reported previously that interferon-alpha (IFN-alpha) induces apoptosis that is counteracted by an epidermal growth factor (EGF) --> Ras --> extracellular signal-regulated kinase (ERK)-dependent survival response in human epidermoid cancer KB cells. We have studied the effects of the cytokine on the cAMP-dependent pathway in these cells. A decrease in the intracellular cAMP levels was recorded in KB cells treated with IFN-alpha, whereas forskolin induced an increase in the production of cAMP that was reduced in the presence of IFN-alpha, suggesting a reduction in the activity of adenylate cyclase (AC) induced by IFN-alpha. These effects were paralleled by significant change in the expression of some AC catalytic subunit(s) and by reduction in the activity of protein kinase A (PKA). 8-Br-cAMP completely antagonized the reduction of PKA activity induced by IFN-alpha, whereas PKA inhibitor KT5720 enhanced the reduction of the enzyme activity induced by IFN-alpha. We have found that IFN-alpha induced a decrease in cAMP response element binding protein (CREB) phosphorylation without changes in its total expression. The concomitant treatment with IFN-alpha and 8-Br-cAMP potentiated and KT5720 counteracted apoptosis induced by IFN-alpha alone. In conclusion, these data suggest that the decrease in AC/cAMP pathway activity is a survival response to the apoptosis induced by IFN-alpha. Therefore, this pathway could represent a target to enhance the antitumor activity of IFN-alpha.

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“…CAMP has been shown to serve as a growth inhibitor in PC3 [Okutani et al, 1991;Bang et al, 19931 and MATLyLu rat prostate cancer cells [Steiner et al,199.51. A causal relationship between the changes in cAMP and 3H-thymidine incorporation in the PC3 cells is not compatible with the fact that in subconfluent cultures (i.e.…”

Section: Discussionmentioning

confidence: 99%

Melatonin receptors in PC3 human prostate tumor cells

Gilad

Laufer²,

Matzkin³

et al. 1999

Journal of Pineal Research

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Melatonin, secreted nocturnally by the pineal gland, can bind to human benign prostate epithelial cells and attenuate their growth and viability. In the present study, melatonin binding and responses were explored in the human steroid-independent PC3 prostatic tumor cells. PC3 cells bound 125I-melatonin with low affinity (Kd ca. 0.9 nM) at high as well as low cell density. Melatonin enhanced cGMP and 3H-thymidine incorporation at low, but attenuated them at high cell density. In addition, melatonin inhibited cAMP at low, but augmented it at high cell density. These effects were associated with an increase in cell count at low- but not high-density cultures. Pertussis toxin treatment suppressed 125I-melatonin binding and ablated all the effects of melatonin on 3H-thymidine incorporation, cAMP, and cGMP at both cell densities. Cholera toxin treatment failed to block the effects of melatonin on 3H-thymidine incorporation, but prevented the modulation by melatonin of cAMP at low and cGMP at high cell density. The cGMP analog 8-Br-cGMP, inhibited melatonin's effects on 3H-thymidine incorporation at both cell densities. H89, a protein kinase A inhibitor, prevented melatonin's effects on 3H-thymidine incorporation at low but not high cell density. These results provide the first demonstration of direct interaction of melatonin with hormone-insensitive prostate tumor cells. The melatonin receptors in the PC3 cells are coupled to pertussis toxin-sensitive G proteins to induce cell density-dependent changes in cGMP, cAMP, and cell growth.

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Role of cyclic AMP and polypeptide growth regulators in growth inhibition by interferon in PC‐3 cells

Cited by 22 publications

References 19 publications

Biological Differences Between Prostate Cancer Cells that Metastasize to Bone Versus Soft Tissue Sites

Biological Differences Between Prostate Cancer Cells that Metastasize to Bone Versus Soft Tissue Sites

Adenylate Cyclase/cAMP Pathway Downmodulation Counteracts Apoptosis Induced by IFN-αin Human Epidermoid Cancer Cells

Melatonin receptors in PC3 human prostate tumor cells

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