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Transforming growth factor-β1 activates interleukin-6 expression in prostate cancer cells through the synergistic collaboration of the Smad2, p38-NF-κB, JNK, and Ras signaling pathways

Park, Jae-Il, Lee, Min-Goo, Cho, Kyucheol, Park, Bum-Joon, Chae, Kwon-Seok, Byun, Do-Sun, Ryu, Byung-Kyu, Park, Yong-Keun, Chi, Sung-Gil·2003·Oncogene
DOI 10.1038/sj.onc.1206478
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Abstract

Transforming growth factor (TGF)-beta1 acts as a potent growth inhibitor of prostate epithelial cells, and aberrant function of its receptor type I and II correlates with tumor aggressiveness. However, intracellular and serum TGF-beta1 levels are elevated in prostate cancer patients and further increased in patients with metastatic carcinoma, suggesting the oncogenic switch of TGF-beta1 role in prostate tumorigenesis. Recently, we reported the mitogenic conversion of TGF-beta1 effect by oncogenic Ha-Ras in prostate cancer cells. Here, we show that TGF-beta1 activates interleukin (IL)-6, which has been implicated in the malignant progression of prostate cancers, via multiple signaling pathways including Smad2, nuclear factor-kappaB (NF-kappaB), JNK, and Ras. TGF-beta1-induced IL-6 gene expression was strongly inhibited by DN-Smad2 but not by DN-Smad3 while it was further activated by wild-type Smad2 transfection. IL-6 activation by TGF-beta1 was accompanied by nuclear translocation of NF-kappaB, which was blocked by the p38 inhibitors SB202190 and SB203580 or by IkappaBalphaDeltaN transfection, indicating the crucial role for the p38-NF-kappaB signaling in TGF-beta1 induction of IL-6. TGF-beta1 activated c-Jun phosphorylation, and IL-6 induction by TGF-beta1 was severely impeded by DN-c-Jun and DN-JNK or AP-1 inhibitor curcumin, showing that the JNK-c-Jun-AP-1 signaling plays a pivotal role in TGF-beta1 stimulation of IL-6. It was also found that the Ras-Raf-MEK1 cascade is ac…

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  • Entire pathways such as MAPK are no longer hijacked for non-canonical induction of TGF-beta, Smad1, and inflammation but instead engage in productive signaling by their cognate ligands, promoting tissue health, regeneration, and homeostatic production of cytokines and growth factors.

    “entire pathways (MAPK, for example) are no longer hijacked for non-canonical induction of TGF-beta, Smad1, and inflammation [57, 58], but instead engage in productive signaling by their cognate ligands, promoting tissue health, regeneration and homeostatic production of cytokines and growth factors [59–61] (with their own positive feed-backs), as we observe.”

    From Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin (2020) · cites this paper as [58]

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Metadata

Authors
Park, J.-I., Lee, M.-G., Cho, K., Park, B.-J., Chae, K.-S., Byun, D.-S., Ryu, B.-K., Park, Y.-K., & Chi, S.-G.
Venue
Oncogene
Publisher
Springer Science and Business Media LLC
Published
2003-07-10
Volume
22
Issue
28
Pages
4314-4332
ISSN
  • 0950-9232
  • 1476-5594
DOI
10.1038/sj.onc.1206478
Cited by
168
References
2
Language
en
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