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The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
Published on: June 16, 2018
SOCS3 as a potential driver of lung metastasis in colon cancer patients
Xuejie Li1, Zuyi Yang2, Bi Chen3,4
1Department of Pathology, The First Affiliated Hospital of Medical School of Zhejiang University, Hangzhou, China.
Background:
The suppressor of cytokine signaling 3 (SOCS3) is the negative feedback regulator of the JAK-STAT signaling pathway. The purpose of our study was to investigate the SOCS3 status in colon primary tumor and lung metastasis and its relationship with macrophages.
Methods:
The SOCS3 expression pattern and its relationship with the immune response in pan-cancer was investigated using multiple methods. Samples and corresponding clinical information of 32 colon cancer patients with lung metastasis were collected, and the CD68, CD163, and SOCS3 status were conducted using immunohistochemistry (IHC). The relationship between SOCS3 status and macrophage markers was analyzed. Besides, we explored the molecular mechanisms of SOCS3 in lung metastasis via the TCGA database.
Results:
High SOCS3 expression was more inclined to poor prognosis and was positively correlated with main immune cell infiltration in almost each cancer type, especially in colon cancer. Compared with the colon primary tumor, lung metastasis harbored higher CD163 and SOCS3 expression, and high SOCS3 expression was more likely to be associated with high CD163 expression in lung metastasis. Besides, the exceptional differentially expressed genes in lung metastasis significantly enriched in immune responses and regulations.
Conclusions:
SOCS3 possessed value as a prognostic marker and target for immunotherapeutic intervention in different tumors and might be a potential target of tumor progression and tumor immunotherapy in colon cancer.
Insights
Suppressor of cytokine signaling 3 (SOCS3) is linked to poorer colon cancer prognosis and increased immune cell infiltration. High SOCS3 and CD163 expression in lung metastasis suggests a role in tumor progression and potential immunotherapy targets.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- The JAK-STAT signaling pathway is crucial in cellular communication and is negatively regulated by suppressor of cytokine signaling 3 (SOCS3).
- Understanding SOCS3's role in cancer, particularly its interplay with immune cells, is vital for developing effective treatments.
Purpose of the Study:
- To investigate the expression patterns of SOCS3 in primary colon tumors and their lung metastases.
- To explore the relationship between SOCS3 status and macrophage markers (CD68, CD163) in colon cancer patients.
- To elucidate the molecular mechanisms of SOCS3 in lung metastasis using TCGA data.
Main Methods:
- Utilized immunohistochemistry (IHC) to assess SOCS3, CD68, and CD163 expression in 32 colon cancer patient samples with lung metastasis.
- Analyzed the correlation between SOCS3 expression and macrophage markers.
- Employed TCGA database to investigate the molecular mechanisms of SOCS3 in lung metastasis.
Main Results:
- Higher SOCS3 expression correlated with poorer prognosis and increased immune cell infiltration across various cancer types, notably colon cancer.
- Lung metastases exhibited higher CD163 and SOCS3 expression compared to primary colon tumors.
- Elevated SOCS3 expression in lung metastasis was associated with increased CD163 expression, suggesting a link with M2 macrophages.
- Differentially expressed genes in lung metastasis were significantly enriched in immune response pathways.
Conclusions:
- SOCS3 demonstrates potential as a prognostic biomarker in various cancers.
- SOCS3 may serve as a therapeutic target for immunotherapeutic interventions, particularly in colon cancer.
- Further research into SOCS3's role in tumor progression and immunotherapy is warranted for colon cancer treatment strategies.
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