Tumor Cell-Derived Complement Component C1r Acts as a Prognostic Biomarker and Promotes Esophageal Squamous Cell Carcinoma Progression
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View abstract on PubMed
Summary
This summary is machine-generated.Complement component C1r is highly expressed in esophageal squamous cell carcinoma (ESCC), promoting tumor progression. Targeting C1r could offer a new therapeutic strategy for ESCC patients.
Area Of Science
- Immunology
- Oncology
- Molecular Biology
Background
- Complement components are increasingly implicated in cancer progression.
- Elevated expression of certain complement components is observed in esophageal squamous cell carcinoma (ESCC).
- The specific roles of these components in ESCC tumorigenesis require further elucidation.
Purpose Of The Study
- To investigate the expression pattern of C1r in ESCC.
- To determine the functional role of C1r in ESCC progression.
- To explore the underlying molecular mechanisms regulated by C1r.
Main Methods
- Analyzed C1r expression in ESCC tissues and cell lines using GEO database and tissue microarrays.
- Utilized single-cell RNA sequencing (scRNA-seq) for detailed analysis of C1r expression in malignant cells.
- Performed C1r knockdown and overexpression experiments in ESCC cells, assessing proliferation, migration, invasion, apoptosis, and in vivo tumor growth.
Main Results
- C1r demonstrated high expression in ESCC tissues and cell lines, correlating with poor prognosis.
- C1r knockdown inhibited ESCC cell proliferation, migration, invasion, and cell-matrix adhesion, while promoting apoptosis.
- C1r knockdown suppressed tumor growth in vivo, and C1r overexpression yielded opposite effects, including induction of MMP-1 and MMP-10.
Conclusions
- C1r is significantly upregulated in ESCC and drives tumor progression.
- C1r acts by inducing matrix metalloproteinases MMP-1 and MMP-10.
- C1r presents a potential prognostic biomarker and therapeutic target for ESCC.
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