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The Soft Agar Colony Formation Assay
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CCT6A Promotes Colon Cancer Cell Proliferation, Migration, and Invasion by Modulating Fatty Acid Metabolism and
Fei Chen1, Caitang Liu2, Rongrong Jiang3
1Department of General Surgery, Linyi Traditional Chinese Medicine Hospital, Linyi, China.
Molecular Carcinogenesis
|December 16, 2025
Summary
Chaperonin containing TCP1 subunit 6A (CCT6A) is elevated in colon cancer, promoting tumor growth and metastasis. Targeting CCT6A may offer a new therapeutic strategy for colon cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Colon cancer presents significant treatment challenges.
- Chaperonin containing TCP1 subunit 6A (CCT6A) is implicated as an oncogene in various cancers.
Purpose of the Study:
- To investigate the role and mechanism of CCT6A in colon cancer progression.
- To evaluate CCT6A as a potential therapeutic target for colon cancer.
Main Methods:
- Analysis of CCT6A expression in colon cancer tissues and cell lines using single-cell datasets, TCGA, immunohistochemistry, qRT-PCR, and Western blot.
- Functional assays including proliferation, migration, invasion, apoptosis, EMT, fatty acid synthesis, and nude mouse models.
- Investigation of the TGF-β1/Smad signaling pathway.
Main Results:
- CCT6A expression is significantly upregulated in colon cancer tissues and correlates with poor prognosis.
- CCT6A enhances colon cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition while suppressing apoptosis.
- CCT6A promotes colon cancer progression by activating the TGF-β1/Smad signaling pathway and modulating fatty acid metabolism.
Conclusions:
- CCT6A acts as an oncogene in colon cancer, driving tumor progression through specific molecular pathways.
- CCT6A represents a promising therapeutic target for colon cancer treatment.
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