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Published on: November 28, 2015
HMGB1: a two-headed signal regulating tumor progression and immunity
Lara Campana1, Lidia Bosurgi, Patrizia Rovere-Querini
1Laboratory of Clinical Immunology, San Raffaele Scientific Institute, DIBIT 3A1, Via Olgettina 58, 20132 Milano, Italy.
Innate immune cells recognize high mobility group box 1 (HMGB1), a damage signal in tumors. This HMGB1 recognition paradoxically promotes tumor growth while also activating anti-cancer T-cell immunity, offering new therapeutic targets.
Area of Science:
- Immunology
- Cancer Biology
- Molecular Medicine
Background:
- Innate immune cells detect extracellular HMGB1 released from damaged cells.
- HMGB1 in tumors has a dual role: promoting angiogenesis and initiating anti-tumor T-cell responses.
- The molecular mechanisms behind HMGB1's contrasting effects are under investigation.
Purpose of the Study:
- To elucidate the dual role of HMGB1 in tumor progression and immune response.
- To explore the involvement of innate receptors, such as TLR4, in cancer therapy.
- To provide insights into the mechanisms of action for conventional cancer treatments.
Main Methods:
- Analysis of HMGB1 recognition by innate immune cells.
- Investigation of HMGB1's impact on tumor neoangiogenesis.
- Assessment of HMGB1's role in anti-neoplastic T-cell responses.
- Study of toll-like receptor 4 (TLR4) involvement in radio- and chemotherapy.
Main Results:
- HMGB1 recognition by innate immunity has paradoxical effects in cancer.
- HMGB1 promotes tumor neoangiogenesis.
- HMGB1 triggers protective anti-neoplastic T-cell responses.
- Innate receptors like TLR4 play a role in conventional cancer treatments.
Conclusions:
- HMGB1's dual role in cancer necessitates a nuanced therapeutic approach.
- Understanding HMGB1-innate receptor interactions can reveal new cancer treatment strategies.
- TLR4 activation by conventional therapies contributes to their efficacy.
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