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MICA/B-driven NK cell dysfunction promotes cervical cancer via Toll signaling
Hatila Tuerxun1, JinQiu Li2, Qian Liu2
1School of Public Health, Xinjiang Medical University and Xinjiang Key Laboratory of Molecular Biology of Endemic Diseases, Urumqi, Xinjiang, 830017, China.
Experimental Cell Research
|December 31, 2025
Summary
MICA/B proteins are highly expressed in cervical cancer (CC) and enhance natural killer (NK) cell anti-tumor immunity. Downregulating MICA/B impairs NK cell function, promoting CC cell growth via the Toll signaling pathway.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Immune status is critical in cervical cancer (CC) development.
- MICA/B proteins are major histocompatibility complex Class I associated proteins that mediate anti-tumor immunity via NK cell receptors.
- Mechanisms of MICA/B in CC progression are not fully understood.
Purpose of the Study:
- To investigate the role of MICA/B in regulating cervical cancer progression.
- To elucidate the mechanisms of MICA/B-mediated anti-tumor immunity in CC.
- To explore MICA/B-NK cell interactions as a potential therapeutic strategy for CC.
Main Methods:
- Spatial transcriptome sequencing and bioinformatics analysis.
- Flow cytometry and cell functional assays.
- Tumor xenograft models in mice.
Main Results:
- MICA/B was highly expressed in CC tissues and cells, correlating with increased NK cell infiltration.
- MICA/B knockdown weakened NK cell activation, enhanced inhibition, reduced cytotoxicity, and altered CC cell proliferation markers (Cyclin, BCL-2/BAX).
- MICA/B regulates inflammatory factors (IL-6, CXCL10/11) via the Toll-like signaling pathway, impacting NK cell function.
Conclusions:
- MICA/B expression on CC cells is pivotal for NK cell-mediated anti-tumor immunity.
- Downregulation of MICA/B attenuates NK cell function, promoting CC cell proliferation and survival through the Toll signaling pathway.
- Targeting MICA/B-NK cell interactions presents a potential therapeutic strategy for cervical cancer.
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