Macrophages affect immune inflammation and proliferation in benign prostatic hyperplasia via androgen receptor and CD40/CD40L signaling pathway

Yang, Minggen; Xu, Zuowei; Zhuang, Zhiming

doi:10.1016/j.tice.2020.101343

Cited by 7 publications

(3 citation statements)

References 30 publications

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“…Further research showed that TEAD directly bound to the promoter region of PRIM1, indicating that PRIM1 was a downstream target of the YAP1/TEAD transcriptional regulatory complex. Aberrant activation of YAP1 signaling is closely related to the initiation and development of multiple tumors [47] , [48] , [49] , including gastric cancer [ 50 , 51 ]. Our experiments found that PRIM1 silencing and verteporfin inhibited cell viability in vitro .…”

Section: Discussionmentioning

confidence: 99%

YAP/TEAD-induced PRIM1 contributes to the progression and poor prognosis of gastric carcinoma

Guo,

Guo

2023

Translational Oncology

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Section: Discussionmentioning

confidence: 99%

YAP/TEAD-induced PRIM1 contributes to the progression and poor prognosis of gastric carcinoma

Guo,

Guo

2023

Translational Oncology

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“…The immune cell infiltration into the prostate was enhanced 44 . Macrophages regulated AR and CD40/CD40L expression to promote inflammation and proliferation as well as inhibit apoptosis of BPH-1 cells through activation of the MAPK signaling pathway 45 . One study analyzed the 50 transurethral prostatic resection specimens, each entailing normal prostate, BPH, and high-grade PC, and evaluated the density and phenotype of the immune cells using IHC methods and immunostaining.…”

Section: Discussionmentioning

confidence: 99%

Exploration of diagnostic biomarkers, microenvironment characteristics, and ursolic acid's therapeutic effect for benign prostate hyperplasia

Chen,

Xu,

et al. 2023

Int. J. Biol. Sci.

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Benign prostatic hyperplasia (BPH) and early-stage prostate cancer (PC) have similar symptoms, making it challenging to differentially diagnose these two conditions. The study used Weighted Gene Co-Expression Network Analysis, as well as two machine learning strategies to identify BPH-specific biomarkers based on an integrated transcriptome data from 922 samples. Eight prognostic genes ( ALCAM , COL6A2 , CRISP2 , FOXF2 , IGF1 , PTN , SCN7A , and UAP1 ) were identified to be BPH-specific biomarkers with high accuracy and specificity. Moreover, we constructed a seven-gene diagnostic classifier to distinguish BPH from PC. The infiltrations of plasmacytoid dendritic cells and neutrophil cells showed distinct differences between BPH and non-BPH groups. Additionally, ursolic acid can reverse transcriptional features associated with the occurrence and progression of BPH. Both in vivo and in vitro experiments have confirmed that it induces apoptosis of BPH cells and inhibits cell proliferation by promoting cell cycle S-phase arrest. The diagnostic biomarkers, microenvironment characteristics, and therapeutic effect of ursolic acid explored in this study offer new diagnostic and therapeutic strategies for BPH.

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“…CD40-CD40L, also known as a pair of costimulatory molecules, is essential for cellular immune responses ( 43 ). It has also been shown to act as an upstream master switch for the MAPK and NF-κB signaling pathways ( 43 – 45 ). Previous studies showed that sCD40L stimulated the secretion of cytokines and HA by up-regulating the phosphorylation levels of MAPK and NF-κB signaling pathways in TAO-OFs ( 27 , 29 , 33 – 36 , 46 ).…”

Section: Discussionmentioning

confidence: 99%

PD-L1 Inhibits T Cell-Induced Cytokines and Hyaluronan Expression via the CD40-CD40L Pathway in Orbital Fibroblasts From Patients With Thyroid Associated Ophthalmopathy

Liu

Mingming

et al. 2022

Front. Immunol.

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Thyroid associated ophthalmopathy (TAO), characterized by T cell infiltration and orbital fibroblast activation, is an organ-specific autoimmune disease which is still short of effective and safety therapeutic drugs. The PD-1/PD-L1 pathway has been reported hindering the progression of Graves’ disease to some extent by inhibiting T cell activity, and tumor therapy with a PD-1 inhibitor caused some adverse effects similar to the symptoms of TAO. These findings suggest that the PD-1/PD-L1 pathway may be associated with the pathogenesis of TAO. However, it remains unknown whether the PD-1/PD-L1 pathway is involved in orbital fibroblast activation. Here, we show that orbital fibroblasts from patients with TAO do not express PD-L1. Based on in vitro OF-T cell co-culture system, exogenous PD-L1 weakens T cell-induced orbital fibroblast activation by inhibiting T cell activity, resulting in reduced production of sICAM-1, IL-6, IL-8, and hyaluronan. Additionally, exogenous PD-L1 treatment also inhibits the expression of CD40 and the phosphorylation levels of MAPK and NF-κB pathways in orbital fibroblasts of the OF-T cell co-culture system. Knocking down CD40 with CD40 siRNA or down-regulating the phosphorylation levels of MAPK and NF-κB pathways with SB203580, PD98059, SP600125, and PDTC can both reduce the expression of these cytokines and hyaluronan. Our study demonstrates that the orbital immune tolerance deficiency caused by the lack of PD-L1 in orbital fibroblasts may be one of the causes for the active orbital inflammation in TAO patients, and the utilization of exogenous PD-L1 to reconstruct the orbital immune tolerance microenvironment may be a potential treatment strategy for TAO.

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Macrophages affect immune inflammation and proliferation in benign prostatic hyperplasia via androgen receptor and CD40/CD40L signaling pathway

Cited by 7 publications

References 30 publications

YAP/TEAD-induced PRIM1 contributes to the progression and poor prognosis of gastric carcinoma

YAP/TEAD-induced PRIM1 contributes to the progression and poor prognosis of gastric carcinoma

Exploration of diagnostic biomarkers, microenvironment characteristics, and ursolic acid's therapeutic effect for benign prostate hyperplasia

PD-L1 Inhibits T Cell-Induced Cytokines and Hyaluronan Expression via the CD40-CD40L Pathway in Orbital Fibroblasts From Patients With Thyroid Associated Ophthalmopathy

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