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Author Spotlight: Unveiling Transmembrane Protein Family-Related Markers in Gastric Cancer and Implications for Targeted Therapies
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Complement C3 overexpression activates JAK2/STAT3 pathway and correlates with gastric cancer progression
Kaitao Yuan1,2, Jinning Ye1,2, Zhenguo Liu3
1Center of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, People's Republic of China.
Journal of Experimental & Clinical Cancer Research : CR
|January 14, 2020
Summary
Localized C3 deposition in gastric cancer (GC) predicts poor survival. This immune signature activates the JAK2/STAT3 pathway, driving tumor progression. Further research is needed to understand this mechanism.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Localized C3 deposition is a known inflammatory factor.
- Its role in gastric cancer (GC) oncoprogression is not fully understood.
- This study investigates the prognostic value and mechanism of C3 deposition in GC.
Purpose of the Study:
- To explore the prognostic value of C3 deposition in GC.
- To elucidate the mechanism of C3-related oncoprogression in GC.
- To investigate the role of C3 in the JAK2/STAT3 signaling pathway in GC.
Main Methods:
- 106 GC patients were prospectively included.
- Regional expression of C3 and effectors in gastric tissues were analyzed using WB, IHC, and qRT-PCR.
- In vitro experiments with GC cell lines investigated the C3-STAT3 signaling pathway.
Main Results:
- C3 and C3a expression were significantly elevated in GC tissues.
- High C3 deposition correlated with advanced pathological T and TNM stages.
- High C3 deposition was an independent predictor of poor 5-year overall survival.
- In vitro, C3 enhanced p-JAK2/p-STAT3 expression in GC cells, dependent on JAK2 activity.
Conclusions:
- Localized C3 deposition serves as a prognostic immune signature in GC.
- Aberrant activation of the JAK2/STAT3 pathway by C3 promotes GC oncoprogression.
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