Dataset Information

ITRAQ-based LC-MS/MS analysis of benign prostatic hyperplasia prostate tissues with different stroma/epithelium ratio

ABSTRACT: To investigate proteins potentially involved in the survival of prostate epithelial cells, we initially collected prostate tissues from 32 BPH patients. Subsequently, we conducted immunohistochemistry (IHC) staining using an anti-alpha-smooth muscle actin (α-SMA) antibody, recognized as a marker for smooth muscle cells and myofibroblasts. We delineated the areas of the stroma, glandular epithelium, and glandular lumen based on this staining. We digitized and conducted subsequent analysis of the relative percentage of different tissue components, including the stroma/epithelium ratio (S/E). Specimens were ranked based on the S/E ratio, leading to the categorization of the 9 specimens with the lowest S/E into group 1 (Epithelium-hi), where the epithelial components may have more significant roles in BPH development. Conversely, the 9 specimens with the highest S/E were placed in group 2 (Epithelium-lo). Within each group, we further subdivided them into 3 subgroups labeled as A through E. Subsequently, we employed isobaric tags for relative and absolute quantitation (iTRAQ)-based liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify the differentially expressed proteins (DEPs) between the two main groups.

ORGANISM(S): Homo Sapiens

SUBMITTER: Jie Jin

PROVIDER: PXD048857 | iProX | Wed Jan 24 00:00:00 GMT 2024

REPOSITORIES: iProX

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Publications

YAP-mediated GPER signaling impedes proliferation and survival of prostate epithelium in benign prostatic hyperplasia.

Liu Zhifu Z Li Senmao S Chen Shengbin S Sheng Jindong J Li Zheng Z Lv Tianjing T Yu Wei W Fan Yu Y Wang Jinlong J Liu Wei W Hu Shuai S Jin Jie J

iScience 20240205 3

Benign prostatic hyperplasia (BPH) occurs when there is an imbalance between the proliferation and death of prostate cells, which is regulated tightly by estrogen signaling. However, the role of G protein-coupled estrogen receptor (GPER) in prostate cell survival remains ambiguous. In this study, we observed that prostates with epithelial hyperplasia showed increased yes-associated protein 1 (YAP) expression and decreased levels of estrogen and GPER. Blocking YAP through genetic or drug interven ...[more]

PMID: 38420594

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Project description:Inflammation has a causal role in many cancers. In prostate cancers, epidemiological data suggest a link between prostatitis and subsequent cancer development, but a proof for this concept in a tumor model has been lacking. A constitutively active version of the IkappaB kinase 2 (IKK2), the molecule activated by a plethora of inflammatory stimuli, was expressed specifically in the prostate epithelium. Signaling of the IKK2/NF-kappaB axis was insufficient for transformation of prostate tissue. However, while PTEN+/- epithelia exhibited intraepithelial neoplasias only recognizable by nuclear alterations, additional IKK2 activation led to an increase in tumor size and formation of cribriform structures and to a fiber increase in the fibroblastic stroma. This phenotype was coupled with inflammation in the prostate gland characterized by infiltration of granulocytes and macrophages. Molecular characterization of the tissues showed a specific loss of smooth muscle markers as well as expression of chemokines attracting immune cells. Isolation of epithelial and stromal cells showed differential chemokine expression by these cells. Correlation studies showed the inflammatory phenotype coupled to loss of smooth muscle in infiltrated glands, but maintenance of the phenotype in glands where inflammation had decreased. Despite the loss of the smooth muscle barrier, tumors were not invasive in a stable genetic background. Data mining revealed that smooth muscle markers are downregulated in human prostate cancers and literature data show that loss of these markers in primary tumors is associated with subsequent metastasis. Our data show that loss of smooth muscle and invasiveness of the tumor are not coupled. Thus, inflammation during early steps of tumorigenesis can lead to increased tumor size and a potential change in the subsequent metastatic potential, but the tumor requires an additional transformation to become a carcinoma. Microarray analysis was used to determine expression differences in lateral prostates from mice with PTEN+/- IKK2ca/ca epithelium (n=3) compared to lateral prostates from mice with PTEN+/- epithelium (n=3).

Dataset Information

ITRAQ-based LC-MS/MS analysis of benign prostatic hyperplasia prostate tissues with different stroma/epithelium ratio

Publications

YAP-mediated GPER signaling impedes proliferation and survival of prostate epithelium in benign prostatic hyperplasia.

Similar Datasets

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