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DEC1 mediates IL-6-induced EMT in CRC via PI3K/AKT/NF-κB activation
Enfang Shan1,2, Weifeng Du1, Ziheng Zhang2
1School of Nursing, Nanjing Medical University, Nanjing, Jiangsu 211166, China.
Journal of Biomedical Research
|August 6, 2026
Summary
Differentiated embryonic chondrocyte expressed gene 1 (DEC1) drives interleukin-6 (IL-6)-induced colorectal cancer (CRC) cell invasion and migration by activating the PI3K/Akt/NF-κB pathway. DEC1 is a key mediator in CRC progression.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Colorectal cancer (CRC) is a significant global health concern.
- Interleukin-6 (IL-6) is implicated in CRC progression.
- The role of differentiated embryonic chondrocyte expressed gene 1 (DEC1) in IL-6-mediated CRC remains unclear.
Purpose of the Study:
- To investigate the role of DEC1 in IL-6-induced invasion and migration of CRC cells.
- To elucidate the underlying molecular mechanisms, including epithelial-to-mesenchymal transition (EMT) and signaling pathways.
Main Methods:
- In vitro studies using CRC cell lines with DEC1 overexpression and knockdown.
- In vivo studies using Dec1 knockout and wild-type CRC mouse models.
- Analysis of EMT markers (E-cadherin, N-cadherin, vimentin) and signaling pathways (PI3K/Akt/NF-κB).
Main Results:
- IL-6 upregulated DEC1, promoting CRC cell invasion and migration by inducing EMT.
- DEC1 overexpression amplified IL-6 effects, while DEC1 knockdown attenuated them.
- DEC1 activation of the PI3K/Akt/NF-κB pathway was crucial for IL-6-induced CRC progression.
- In vivo studies confirmed DEC1's role in enhancing tumor invasion and metastasis.
Conclusions:
- DEC1 mediates IL-6-induced invasion and migration in colorectal cancer.
- The PI3K/Akt/NF-κB signaling pathway is a key mechanism through which DEC1 exerts its effects.
- Targeting DEC1 may offer a therapeutic strategy for advanced CRC.
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