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Published on: December 13, 2019
HMGB3 is a Potential Therapeutic Target by Affecting the Migration and Proliferation of Colorectal Cancer
Wenjing Gong1, Yang Guo1, Hang Yuan1
1General Surgery, Cancer Center, Department of Colorectal Surgery, Zhejiang Provincial People's Hospital, Affiliated People's Hospital of Hangzhou Medical College, Hangzhou, China.
Abstract:
Colorectal cancer is one of the common malignant tumors in the digestive system, with high incidence and mortality rate. Therefore, there is an urgent need to identify and develop new molecular targets for colorectal cancer treatment. Previous studies have pointed out the important role of HMGB3 in tumors, and how it works in colorectal cancer needs to be studied in depth. In this study, we found that HMGB3 was highly expressed in COAD in the cBioPortal and GEPIA2 databases. Kaplan-Meier analysis showed that compared with patients with lower HMGB3 levels, patients with higher HMGB3 levels had poorer OS (p = 0.001). We also found a correlation between HMGB3 expression and immune infiltration of CRC. To investigate the mechanism of HMGB3 knockdown-mediated colorectal cancer inhibition, we detected a downregulation of N-cadherin, Vimentin and β-catenin proteins after knockdown of HMGB3. Taken together, HMGB3 can be an effective target for CRC treatment in the future, and we have reason to believe that HMGB3 will be of greater value in more tumors in the near future.
Insights
High mobility group box 3 (HMGB3) is overexpressed in colorectal cancer (CRC), correlating with poor survival and immune infiltration. HMGB3 inhibition reduces tumor cell markers, suggesting it as a potential therapeutic target for CRC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Colorectal cancer (CRC) presents a significant global health challenge due to its high incidence and mortality.
- Identifying novel molecular targets is crucial for advancing CRC treatment strategies.
- High mobility group box 3 (HMGB3) has been implicated in tumorigenesis, necessitating a deeper understanding of its role in CRC.
Purpose of the Study:
- To investigate the expression levels and clinical significance of HMGB3 in colorectal adenocarcinoma (COAD).
- To explore the correlation between HMGB3 expression and immune infiltration in CRC.
- To elucidate the underlying molecular mechanisms of HMGB3's function in CRC progression.
Main Methods:
- Utilized cBioPortal and GEPIA2 databases to analyze HMGB3 expression in COAD.
- Performed Kaplan-Meier survival analysis to assess the relationship between HMGB3 levels and overall survival (OS).
- Investigated the impact of HMGB3 knockdown on key proteins involved in cell adhesion and migration (N-cadherin, Vimentin, β-catenin).
Main Results:
- HMGB3 was found to be significantly upregulated in COAD tissues compared to normal tissues.
- Higher HMGB3 expression was strongly associated with poorer OS in CRC patients (p = 0.001).
- HMGB3 expression correlated with specific patterns of immune infiltration within the CRC microenvironment.
- Knockdown of HMGB3 led to the downregulation of N-cadherin, Vimentin, and β-catenin proteins.
Conclusions:
- HMGB3 is a promising biomarker for predicting poor prognosis in colorectal cancer.
- HMGB3 plays a role in CRC progression, potentially through regulating proteins involved in epithelial-mesenchymal transition.
- HMGB3 represents a potential therapeutic target for future colorectal cancer treatments.
