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Updated: Apr 19, 2026
Quantitation of Protein Expression and Co-localization Using Multiplexed Immuno-histochemical Staining and Multispectral Imaging
Published on: April 8, 2016
Differential expression of MST4, STK25 and PDCD10 between benign prostatic hyperplasia and prostate cancer
Heyu Zhang1, Xi Ma2, Saihui Peng3
1Department of Immunology, School of Basic Medical Sciences, Peking University No. 38 Xueyuan Road, Beijing, PR China ; Human Disease Genomics Center, Peking University 38 Xueyuan Road, Beijing, PR China ; Central Laboratory, Peking University School of Stomatology 22 South Zhongguancun Road, Beijing, PR China.
Abstract:
Both benign prostatic hyperplasia (BPH) and prostate cancer (PC) are common diseases for men around the world. Both serine/threonine protein kinase MST4 (MST4) and serine/threonine kinase 25 (STK25) belong to the Ste20-like kinases and interact with programmed cell death 10 (PDCD10) which is closely linked to cancer diseases. To clarify the roles of MST4, STK25 and PDCD10 in prostate carcinogenesis, we examined MST4, STK25 and PDCD10 expression in tissue microarray blocks containing 110 cores of BPH and 160 cores of PC immunohistochemically and evaluated their correlation with clinicopathological findings. MST4 was not expressed in all the BPH cases and expressed in 38.7% of PC cases (P < 0.0001). STK25 expression was found in 77.3% of BPH cases and 93.1% of PC cases (P < 0.0001). PDCD10 staining was considered weak in 82 (74.5%) and strong in 28 (25.5%) of BPH cases. However, in prostate cancer cases, PDCD10 staining was weak in 95 (59.4%) and strong in 65 (40.6%) (P < 0.05). PDCD10 and STK25 immunostaining were associated with age in prostatic hyperplasia cases (P < 0.05). The staining intensity for STK25 was significantly greater in Gleason grades 3-5 (47.1% of such cases staining strongly) compared with other grades of prostate cancer (only 26.5% of these cases staining strongly; P < 0.05). Our results suggest that MST4, STK25 and PDCD10 are unregulated in prostate cancer and may play roles in prostate tumorigenesis. MST4 may be a helpful marker for identifying prostate cancer.
Insights
Serine/threonine kinase MST4 (MST4) and STK25, along with PDCD10, are implicated in prostate cancer development. MST4 shows promise as a biomarker for identifying prostate cancer, while STK25 and PDCD10 expression correlates with disease progression.
Area of Science:
- Urology
- Oncology
- Molecular Biology
Background:
- Benign prostatic hyperplasia (BPH) and prostate cancer (PC) are prevalent globally.
- Serine/threonine protein kinase MST4 (MST4) and STK25 are Ste20-like kinases interacting with programmed cell death 10 (PDCD10), a molecule linked to cancer.
Purpose of the Study:
- To investigate the expression and clinical significance of MST4, STK25, and PDCD10 in prostate carcinogenesis.
- To determine the correlation between these proteins and clinicopathological features of BPH and PC.
Main Methods:
- Immunohistochemical analysis of MST4, STK25, and PDCD10 expression in tissue microarrays.
- Evaluation of 110 BPH and 160 PC tissue cores.
- Correlation analysis with clinicopathological findings.
Main Results:
- MST4 was significantly upregulated in PC compared to BPH (38.7% vs. 0%, P < 0.0001).
- STK25 expression was higher in PC (93.1%) than BPH (77.3%) (P < 0.0001) and associated with higher Gleason grades.
- PDCD10 expression showed a trend towards stronger staining in PC (40.6%) versus BPH (25.5%) (P < 0.05).
Conclusions:
- MST4, STK25, and PDCD10 are dysregulated in prostate cancer and may contribute to tumorigenesis.
- MST4 demonstrates potential as a diagnostic marker for prostate cancer.
- STK25 and PDCD10 expression levels correlate with disease characteristics, suggesting roles in prostate cancer progression.
