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Aldolase A Promotes Colorectal Cancer Progression through Targeting COPS6 and Regulating MAPK Signaling Pathway
Ya Lu1, Yuan Zhang1, Xinyue Wang1
1Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.
Aldolase A (ALDOA) promotes colorectal cancer (CRC) progression by enhancing cell proliferation and metastasis. Targeting ALDOA and its interaction with COPS6 may offer new therapeutic strategies for CRC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Colorectal cancer (CRC) poses a significant health risk, with its underlying molecular mechanisms requiring further elucidation.
- Aldolase A (ALDOA) is implicated in various cancers, but its specific role and mechanisms in CRC remain largely unknown.
Purpose of the Study:
- To investigate the role and molecular mechanisms of Aldolase A (ALDOA) in the progression of colorectal cancer (CRC).
- To identify potential therapeutic targets and biomarkers for CRC based on ALDOA's function.
Main Methods:
- Analysis of ALDOA expression and enzymatic activity in CRC tissues and cell lines.
- In vitro and in vivo experiments involving ALDOA gene silencing.
- Immunoprecipitation assays and mass spectrometry to identify ALDOA-interacting proteins.
- Investigation of ALDOA's effects on epithelial-mesenchymal transition (EMT) and MAPK signaling pathways.
Main Results:
- High ALDOA expression and enzymatic activity were observed in CRC tissues and cells.
- ALDOA silencing significantly inhibited CRC cell proliferation and metastasis both in vitro and in vivo.
- COPS6 was identified as a binding protein of ALDOA, and its depletion reversed ALDOA-mediated CRC progression.
- ALDOA overexpression was found to activate EMT and the MAPK signaling pathway.
Conclusions:
- ALDOA promotes CRC proliferation and metastasis by interacting with COPS6, inducing EMT, and activating the MAPK pathway.
- ALDOA represents a promising potential biomarker and therapeutic target for colorectal cancer.
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