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Furthermore, the targeting HMGB1 in clinical trials has been carried out vigorously. Several clinical studies
have shown that HMGB1 is a promising biomarker for a variety of cancer types. For example, HMGB1 was
reported to link hepatocyte injury to ductular reactions, hepatocyte metaplasia, and
[79]
hepatocarcinogenesis . The release of HMGB1 in response to proapoptotic glioma killing strategies
exhibited high efficacy and safety profile because its blockade with glycyrrhizin completely blocked tumor
[80]
regression . These clinical trials could lead to exploring potential cure strategies for cancers harboring high
levels of HMGB1 expression including PCa.
CONCLUSION
From recent studies, evidence on the prominent functions of HMGB1 in the development of cancer is
rapidly accumulating. Studies from others and our group indicate that HMGB1 may also play a crucial role
in PCa progression. The interaction of HMGB1 with RAGE indicates a central role of HMGB1 in PCa
progression. Preclinical studies also support that HMGB1 is upregulated in PCa patients and potentially acts
as a novel prognostic biomarker for overall survival of PCa patients. Importantly, identification of the
molecules that control the status of HMGB1 would both add to the understanding of the regulation role of
HMGB1 and potentially provide additional targeted approaches for the therapeutic manipulation of
HMGB1, which may ultimately lead to the improvement of effective therapy for PCa patients. In addition,
combining hormonal therapy with agents which target HMGB1 may provide novel avenues for therapeutic
development against PCa. Nevertheless, further advanced analysis of HMGB1 and elucidation of the
complicacy of the intracellular and extracellular roles of HMGB1 will give us with the knowledge to further
improve the development of effective HMGB1-related anti-cancer therapies. Being easily accessible from
body serum, HMGB1 has great potential to become a promising and viable tool for early diagnosis and
targeted therapy of cancer.
DECLARATIONS
Authors’ contributions
The author contributed solely to the article.
Availability of data and materials
Not applicable.
Financial support and sponsorship
None.
Conflicts of interest
The author declared that there are no conflicts of interest.
Ethical approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Copyright
© The Author(s) 2021.