CEACAM7 enhances oral cancer metastasis by upregulating CD317 expression
- Chun-Wen Su 1, Wei-En Yang 1, Yi-Hsien Hsieh 1, Chih-Hsin Tang 2, Chiao-Wen Lin 3, Shun-Fa Yang 1
- Chun-Wen Su 1, Wei-En Yang 1, Yi-Hsien Hsieh 1
- 1Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
- 2Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan; Department of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan; Chinese Medicine Research Center, China Medical University, Taichung, Taiwan.
- 3Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan; Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan.
- 0Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
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View abstract on PubMed
Summary
This summary is machine-generated.Carcinoembryonic antigen-related cell adhesion molecule 7 (CEACAM7) promotes oral cancer metastasis by upregulating CD317 via p-JNK and p-Src pathways. CEACAM7 and CD317 are potential therapeutic targets for metastatic oral cancer.
Area Of Science
- Oncology
- Molecular Biology
- Cell Biology
Background
- Carcinoembryonic antigen-related cell adhesion molecule 7 (CEACAM7) is implicated in cancer progression, but its role in oral cancer metastasis is unclear.
- Understanding CEACAM7's function is crucial for developing targeted therapies for oral squamous cell carcinoma.
Purpose Of The Study
- To investigate the role of CEACAM7 in the development and metastasis of oral cancer.
- To identify the molecular mechanisms underlying CEACAM7-mediated oral cancer cell migration.
- To explore CEACAM7 and its associated molecules as potential therapeutic targets.
Main Methods
- Analysis of Gene Expression Omnibus (GEO) database for CEACAM7 expression in oral cancer.
- RNA sequencing to identify downstream targets of CEACAM7.
- Transwell migration/invasion assays, western blotting, and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to assess cell migration and protein expression.
- Pharmacological inhibition of JNK and Src pathways.
- Validation using xenograft models and clinical tissue specimens.
Main Results
- Elevated CEACAM7 expression in advanced oral cancer correlates with lymph node metastasis and poorer survival.
- CEACAM7 overexpression upregulates CD317 expression, enhancing oral cancer cell migration.
- CD317 knockdown suppresses oral cancer cell migration.
- CEACAM7 regulates CD317 and cell migration via phosphorylated JNK (p-JNK) and Src (p-Src) signaling pathways.
- In vivo and clinical data confirm the roles of CEACAM7 and CD317 in oral cancer metastasis.
Conclusions
- CEACAM7 promotes oral cancer metastasis by upregulating CD317 through the p-JNK and p-Src signaling pathways.
- CEACAM7 and CD317 represent promising therapeutic targets for treating metastatic oral cancer.
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