Integrating the dysregulated inflammasome-based molecular functionome in the malignant transformation of endometriosis-associated ovarian carcinoma

Chia-Ming Chang, Mong‐Lien Wang, Mong-Lien Wang, Kai-Hsi Lu, Yi‐Ping Yang, Yi-Ping Yang, Chi-Mou Juang, Chi‐Mou Juang, Peng‐Hui Wang, Peng-Hui Wang, Ren-Jun Hsu, Ren‐Jun Hsu, Mu-Hsien Yu, Cheng‐Chang Chang, Cheng-Chang Chang
Oncotarget · 2017 · vol. 9(3) , pp. 3704–3726 · doi:10.18632/oncotarget.23364 · PMID:29423077 · PMC5790494 · W2780548642
article OA: gold CC0 ⤵ 12 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study integrated gene expression data to identify an inflammasome-based molecular functionome dysregulated in endometriosis-associated ovarian carcinoma, linking specific inflammasome genes to patient survival.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study examined molecular changes underlying the malignant transformation from endometriosis (ES) to endometriosis-associated ovarian carcinoma (EAOC) by applying a gene set regularity (GSR) model to microarray datasets for ES, clear cell carcinoma (CCC), and endometrioid carcinoma (EC), followed by integrative identification of differentially expressed genes within deregulated GO-based functionomes. Across 39 GEO datasets (107 ES, 85 CCC, 90 EC, and matched normal controls), functionome regularity was broadly deteriorated in ES/CCC/EC versus controls, and machine-learning classification using GSR indices achieved very high accuracy; the authors note a caveat that analyses depend on the harmonization of gene sets across multiple microarray platforms and use of shared genesets. Immune/inflammation-related dysregulated functions were prominent, and inflammasome-related genes including NLRP3, AIM2, PYCARD, NAIP, TNF, TLR1, TLR7, TOLLIP, and NFKBIA were differentially expressed and correlated with poor progression-free survival, with immunohistochemistry confirming expression trends in ES/CCC/EC specimens. This paper is centrally about endometriosis — it specifically analyzes inflammasome-based immune/inflammation functionome dysregulation driving malignant transformation from endometriosis to EAOC (CCC/EC).

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Abstract

The coexistence of endometriosis (ES) with ovarian clear cell carcinoma (CCC) or endometrioid carcinoma (EC) suggested that malignant transformation of ES leads to endometriosis associated ovarian carcinoma (EAOC). However, there is still lack of an integrating data analysis of the accumulated experimental data to provide the evidence supporting the hypothesis of EAOC transformation. Herein we used a function-based analytic model with the publicly available microarray datasets to investigate the expression profiling between ES, CCC, and EC. We analyzed the functional regularity pattern of the three type of samples and hierarchically clustered the gene sets to identify key mechanisms regulating the malignant transformation of EAOC. We identified a list of 18 genes (NLRP3, AIM2, PYCARD, NAIP, Caspase-4, Caspase-7, Caspase-8, TLR1, TLR7, TOLLIP, NFKBIA, TNF, TNFAIP3, INFGR2, P2RX7, IL-1B, IL1RL1, IL-18) closely related to inflammasome complex, indicating an important role of inflammation/immunity in EAOC transformation. We next explore the association between these target genes and patient survival using Gene Expression Omnibus (GEO), and found significant correlation between the expression levels of the target genes and the progression-free survival. Interestingly, high expression levels of AIM2 and NLRP3, initiating proteins of inflammasomes, were significantly correlated with poor progression-free survival. Immunohistochemistry staining confirmed a correlation between high AIM2 and high Ki-67 in clinical EAOC samples, supporting its role in disease progression. Collectively, we established a bioinformatic platform of gene-set integrative molecular functionome to dissect the pathogenic pathways of EAOC, and demonstrated a key role of dysregulated inflammasome in modulating the malignant transformation of EAOC.

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endometriosis

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