New progress with calcium-binding protein S100A16 in digestive system disease

ABSTRACT

Introduction

This review summarizes and analyzes the abnormal expression and mechanism of S100A16 in digestive system diseases, which is expected to provide new ideas and methods for adjuvant treatment and prognosis evaluation of digestive system diseases.

Areas covered

Based on original publications found in database systems (PubMed, Cochrane), we introduce the mechanism and research progress of S100A16 in digestive system tumors, inflammatory bowel disease and fatty liver.

Expert opinion

S100A16 is closely related to the proliferation, migration, and invasion of digestive system tumor cells. Further, it plays an important role in inflammatory bowel disease and fatty liver.

KEYWORDS:

• S100A16
• calcium-binding protein
• colorectal cancer
• pancreatic cancer
• digestive system

Article highlights

• Calcium-binding protein S100A16, the 20th member of the S100 family, is closely related to proliferation, migration, and invasion of tumor cells and may have significant effects on digestive system diseases.

• The upregulation of S100A16 expression may accelerate the progression of gastric cancer through the EMT process.

• S100A16 is involved in the regulation of several related cell pathways contributing to the pathogenesis of pancreatic cancer.

• The expression of S100A16 is negatively correlated with the progression of colorectal cancer and Crohn’s disease, which may be respectively related to JNK/p38MAPK signaling pathway and innate immunity, respectively.

• The relationship between S100A16 and HCC has not been studied clearly, as only one study has shown that S100A16 is upregulated and can be used to construct a prognostic model in HCC.

Acknowledgments

We acknowledge all authors who participated in the preparation, collation, and writing of the review. We thank the Biorender [https://app.biorender.com/] which is an online tool for helping us create beautiful and professional figures. We also acknowledge Xiangya School of Medicine, Central South University for its help and support.

Declaration of interests

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This work was supported by funding from the National Natural Science Foundation of China (No.81770306, No. 81971820).