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Updated: Jan 28, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
Estrogen receptors participate in carcinogenesis signaling pathways by directly regulating NOD-like receptors
Wentao Fan1, Xiaona Gao1, Chenchen Ding1
1College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China; MOE Joint International Research Laboratory of Animal Health and Food Safety, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
Abstract:
Increasing evidence indicates that the NOD-like receptors (NLRs) family may act as critical back-up defenses and provide synergistic responses when confronted with persistent danger. However, the precise regulatory mechanism of NLRs and the contribution of NLRs to cancer are still unknown. In our previous study, we found that estrogen receptors (ERs) have a close connection with NLRs in the inflammatory response. Here, ERs are first identified as NLRs transcription regulation factors, both regulate NLRs expression and promote inflammasome co-localization. Furthermore, we identified that NLRP3 was differentially expressed in colon normal and cancer cells, selective ERα antagonist could significantly decrease pro-inflammatory cytokines expression, suppress proliferation and promote apoptosis by inhibited NLRP3 expression and inflammasome activity. In short, the research demonstrates that ERs participate in the NLR-associated signaling pathway in cancer by directly regulating NLRs. Our results provide novel insight into ERs as therapeutic targets in NLR-related inflammation and cancer.
Insights
Estrogen receptors (ERs) regulate NOD-like receptors (NLRs) in cancer. Targeting ERs may treat NLR-related inflammation and colon cancer by inhibiting NLRP3 inflammasome activity.
Area of Science:
- Immunology
- Molecular Biology
- Oncology
Background:
- NOD-like receptors (NLRs) are crucial for innate immunity and inflammation.
- The precise regulatory mechanisms of NLRs and their role in cancer remain incompletely understood.
- Estrogen receptors (ERs) have previously shown connections with NLRs in inflammatory responses.
Purpose of the Study:
- To elucidate the regulatory role of Estrogen Receptors (ERs) in NOD-like Receptors (NLRs) signaling.
- To investigate the involvement of ERs and NLRs, specifically NLRP3, in colon cancer development.
- To explore the therapeutic potential of targeting ERs in NLR-associated inflammation and cancer.
Main Methods:
- Investigated ERs as transcription factors for NLRs.
- Analyzed NLRP3 expression in normal and colon cancer cells.
- Utilized selective ERα antagonists to assess effects on pro-inflammatory cytokines, proliferation, and apoptosis.
Main Results:
- ERs were identified as direct regulators of NLRs transcription and inflammasome co-localization.
- NLRP3 showed differential expression in colon normal versus cancer cells.
- ERα antagonism reduced pro-inflammatory cytokines, suppressed proliferation, and promoted apoptosis via NLRP3 inhibition.
Conclusions:
- Estrogen receptors directly regulate NLRs, influencing the NLR-associated signaling pathway in cancer.
- NLRP3 inflammasome activity is implicated in colon cancer progression.
- ERs represent a promising therapeutic target for NLR-related inflammation and colon cancer.
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