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Updated: Oct 1, 2025
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Indolethylamine-N-Methyltransferase Inhibits Proliferation and Promotes Apoptosis of Human Prostate Cancer Cells: A
Wang Jianfeng1, Wang Yutao1, Bi Jianbin1
1Department of Urology, The First Hospital of China Medical University, Shenyang, China.
Abstract:
Indolethylamine-N-methyltransferase (INMT) is a methyltransferase downregulated in lung cancer, meningioma, and prostate cancer; however, its role and mechanism in prostate cancer remain unclear. By analyzing The Cancer Genome Atlas (TCGA)-PRAD, we found that the expression of INMT in prostate cancer was lower than that of adjacent non-cancerous prostate tissues and was significantly correlated with lymph node metastasis Gleason score, PSA expression, and survival. Combined with the GSE46602 cohorts for pathway enrichment analysis, we found that INMT was involved in regulating the MAPK, TGFβ, and Wnt signaling pathways. After overexpression of INMT in prostate cancer cell lines 22Rv1 and PC-3, we found an effect of INMT on these tumor signal pathways; overexpression of INMT inhibited the proliferation of prostate cancer cells and promoted apoptosis. Using the ESTIMATE algorithm, we found that with the increase of INMT expression, immune and stromal scores in the tumor microenvironment increased, immune response intensity increased, and tumor purity decreased. The difference in INMT expression affected the proportion of several immune cells. According to PRISM and CTRP2.0, the potential therapeutic agents associated with the INMT expression subgroup in TCGA were predicted. The area under the curve (AUC) values of 26 compounds positively correlated with the expression of INMT, while the AUC values of 14 compounds were negatively correlated with the expression of INMT. These findings suggest that INMT may affect prostate cancer's occurrence, development, and drug sensitivity via various tumor signaling pathways and tumor microenvironments.
Insights
Indolethylamine-N-methyltransferase (INMT) is downregulated in prostate cancer, impacting tumor growth and apoptosis. Its expression influences the tumor microenvironment and potential drug sensitivity, suggesting a key role in cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genomics
Background:
- Indolethylamine-N-methyltransferase (INMT) is a methyltransferase known to be downregulated in several cancers.
- Its specific role and underlying mechanisms in prostate cancer progression are not well understood.
Purpose of the Study:
- To investigate the role of INMT in prostate cancer.
- To elucidate the molecular mechanisms by which INMT influences prostate cancer development, tumor microenvironment, and drug sensitivity.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA)-PRAD and GSE46602 datasets for INMT expression and correlation with clinical parameters.
- Pathway enrichment analysis to identify INMT-associated signaling pathways (MAPK, TGFβ, Wnt).
- In vitro experiments involving INMT overexpression in prostate cancer cell lines (22Rv1, PC-3).
- Assessment of tumor microenvironment characteristics using the ESTIMATE algorithm.
- Prediction of potential therapeutic agents based on INMT expression subgroups using PRISM and CTRP2.0 databases.
Main Results:
- INMT expression is significantly lower in prostate cancer tissues compared to adjacent non-cancerous tissues.
- Decreased INMT expression correlates with lymph node metastasis, Gleason score, PSA levels, and poorer survival.
- INMT overexpression inhibits prostate cancer cell proliferation and promotes apoptosis.
- INMT influences MAPK, TGFβ, and Wnt signaling pathways.
- Increased INMT expression is associated with higher immune and stromal scores, enhanced immune response, and decreased tumor purity.
- INMT expression levels correlate with the sensitivity to various potential therapeutic agents.
Conclusions:
- INMT plays a significant role in the development and progression of prostate cancer.
- INMT impacts prostate cancer through modulation of key signaling pathways and the tumor microenvironment.
- INMT expression levels may serve as a predictive biomarker for drug sensitivity in prostate cancer.
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