Cytokine Variations in Patients With Hormone Treated Prostate Cancer

Wise, Gilbert J.; Marella, Venkata K.; Talluri, Giridhar; Shirazian, Djamshid

doi:10.1097/00005392-200009010-00024

Cited by 68 publications

(44 citation statements)

References 13 publications

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“…36). Large amounts of T H 2 cytokines are observed in the tumor microenvironment and peripheral blood of patients with prostate, bladder and breast cancers [37][38][39] . IL-4 can directly induce the proliferation of colon, breast, head and neck, ovarian and prostate cancer cells in vitro [40][41][42] and can also activate myeloid cell-derived suppressor cells 43 or type 2 tumor-associated macrophages 44 and inhibit T H 1 polarization.…”

Section: Discussionmentioning

confidence: 99%

The receptor NLRP3 is a transcriptional regulator of TH2 differentiation

et al. 2015

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The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1β (IL-1β) and IL-18. Whether NLRP3 can shape immunological function independently of inflammasomes is unclear. We found that NLRP3 expression in CD4(+) T cells specifically supported a T helper type 2 (TH2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a TH2 program. In TH2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient TH2 cells supported melanoma tumor growth in an IL-4-dependent manner and also promoted asthma-like symptoms. Our results demonstrate the ability of NLRP3 to act as a key transcription factor in TH2 differentiation.

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Section: Discussionmentioning

confidence: 99%

The receptor NLRP3 is a transcriptional regulator of TH2 differentiation

et al. 2015

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“…Yet another IL, IL-4 was not only found in the serum of patients with hormone refractory prostate cancers but also proved to be able to activate AR in the absence of androgens (27,124). This depends on Akt because its inhibition blocks the activation of AR by IL-4 (27).…”

Section: Cytokinesmentioning

confidence: 99%

Minireview: Tipping the Balance: Ligand-Independent Activation of Steroid Receptors

Bennesch

Picard

2015

Molecular Endocrinology

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Steroid receptors are prototypical ligand-dependent transcription factors and a textbook example for allosteric regulation. According to this canonical model, binding of cognate steroid is an absolute requirement for transcriptional activation. Remarkably, the simple one ligand-one receptor model could not be farther from the truth. Steroid receptors, notably the sex steroid receptors, can receive multiple inputs. Activation of steroid receptors by other signals, working through their own signaling pathways, in the absence of the cognate steroids, represents the most extreme form of signaling cross talk. Compared with cognate steroids, ligand-independent activation pathways produce similar but not identical outputs. Here we review the phenomena and discuss what is known about the underlying molecular mechanisms and the biological significance. We hypothesize that steroid receptors may have evolved to be trigger happy. In addition to their cognate steroids, many posttranslational modifications and interactors, modulated by other signals, may be able to tip the balance.

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“…One proposed explanation is that several cytokines such as interleukin-6, tumor necrosis factor-alpha, and vascular endothelial growth factor initiate glandular epithelial proliferation and destruction, leading to increases in serum PSA [21,22]. In addition, inflammation also triggers the production of alpha-1-antichymotrypsin from the liver as a typical reaction to inflammation, which binds to PSA [23]. Therefore, the %fPSA level will decrease despite an increase in fPSA.…”

Section: Commentmentioning

confidence: 99%