Tumor cell-derived DNASE2B mediates M2 macrophage infiltration to promote prostate cancer progression through the PSA secretion
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View abstract on PubMed
Summary
This summary is machine-generated.High deoxyribonuclease II beta (DNASE2B) expression in prostate cancer promotes tumor growth by increasing M2 macrophage infiltration and PSA secretion. Silencing DNASE2B inhibits cancer progression, revealing a key mechanism in prostate cancer development.
Area Of Science
- Oncology
- Molecular Biology
- Immunology
Background
- Prostate cancer (PCa) progression is driven by unclear mechanisms.
- Deoxyribonuclease II beta (DNASE2B) is overexpressed in PCa, suggesting a potential role in disease advancement.
Purpose Of The Study
- To investigate the role of DNASE2B in prostate cancer progression.
- To elucidate the underlying mechanisms of DNASE2B-mediated PCa advancement, including its impact on the immune microenvironment and PSA secretion.
Main Methods
- Analysis of DNASE2B expression in TCGA database, PCa cell lines, and tissues using Western blotting, q-PCR, and immunohistochemistry.
- Functional assays (cell scratch, Transwell, subcutaneous tumor assays) to assess biological functions.
- Immune microenvironment analysis using TISCH2, GEO datasets, Timer2.0, and validation of M2 macrophage infiltration via multiple methods.
- Identification of downstream targets and verification of the DNASE2B-PSA relationship using q-PCR, Western blotting, and ELISA.
Main Results
- DNASE2B expression is significantly elevated in PCa tissues compared to normal tissues.
- Silencing DNASE2B inhibited PCa cell proliferation and tumor growth in vitro and in vivo.
- DNASE2B expression positively correlated with M2 macrophage infiltration and PSA secretion, which collectively accelerate PCa progression.
Conclusions
- Elevated DNASE2B expression drives prostate cancer progression.
- DNASE2B enhances M2 macrophage infiltration and accelerates PCa by increasing PSA secretion.
- Targeting DNASE2B may represent a therapeutic strategy for prostate cancer.
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