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Published on: January 5, 2017
Sensory nerves unlock the TOLL-7 gate for cancer spread
R K Subbarao Malireddi1, Thirumala-Devi Kanneganti1
1Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Abstract:
Cancers hijack the nervous system for growth and spread. Thus, disrupting neuron-cancer crosstalk holds promise for blocking metastasis. Recently, Padmanaban et al. reported new therapeutic targets and showed that breast cancer cells activate sensory neurons to secrete the neuropeptide substance P (SP), leading to single-strand (ss)RNA release and noncanonical Toll-like receptor (TLR)7 signaling that drives metastasis.
Insights
Cancers exploit nerve cells to grow and spread. Disrupting this communication by targeting sensory neuron activation and substance P (SP) release may block cancer metastasis.
Area of Science:
- Neuroscience
- Oncology
- Immunology
Background:
- Cancers utilize neural pathways for progression and metastasis.
- Interfering with neuron-cancer interactions presents a potential anti-metastasis strategy.
Purpose of the Study:
- To identify and validate novel therapeutic targets for blocking cancer metastasis.
- To elucidate the role of sensory neurons and substance P in cancer progression.
Main Methods:
- Investigated the activation of sensory neurons by breast cancer cells.
- Analyzed the release of neuropeptide substance P (SP) and its downstream effects.
- Examined the role of single-strand RNA (ssRNA) and Toll-like receptor 7 (TLR7) signaling in metastasis.
Main Results:
- Breast cancer cells activate sensory neurons, inducing the secretion of substance P (SP).
- This process leads to the release of single-strand RNA (ssRNA).
- The released ssRNA activates noncanonical Toll-like receptor 7 (TLR7) signaling, promoting metastasis.
Conclusions:
- Neuron-cancer crosstalk, specifically through SP and TLR7 signaling, is a key driver of metastasis.
- Targeting this pathway offers a promising therapeutic approach to inhibit cancer spread.
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