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DHA inhibits invasion and metastasis in NSCLC cells by interfering with CCL18/STAT3 signaling pathway
Hai-Qing Luo1, Yu-Meng Huang2, Jing Li3,4
1Center of Oncology, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, People's Republic of China. hqluo@126.com.
Abstract:
Omega-3 has been proposed as an antitumor substance that suppresses the growth and metastasis of multiple types of tumor cells, including lung cancer, but the specific mechanisms involved remain obscure. Our previous studies showed that the expression of chemokine ligand 18 was related to the migration and metastasis of non-small cell lung cancer. Here, we aim to explore whether omega-3 inhibits invasion and metastasis of NSCLC by regulating the expression of CCL18. The expression of CCL18, metastasis- and epithelial-mesenchymal transition (EMT)-related genes at mRNA and protein levels in NSCLC cell lines were detected by RT-qPCR and Western blot, respectively. The metastatic and invasive capability of NSCLC cells were evaluated by scratch wound healing and Transwell assays, respectively. Our results showed that the level of CCL18 is positively associated with metastatic ability of NSCLC cells. Docosahexaenoic acid, an important long-chain, polyunsaturated omega-3 (n-3) fatty acid, significantly inhibited invasion and metastasis of NSCLC cells, and concomitantly downregulated the expression of metastasis- and EMT-related genes and p-STAT3 signaling pathway. Additionally, we found that DHA inhibited CCL18 expression in lung cancer cells, while overexpression of CCL18 effectively reversed DHA-mediated downregulation in the expression of metastasis- and EMT-related genes and p-STAT3 signaling as well as DHA-mediated inhibitory effect on metastasis and invasion of NSCLC cells. DHA inhibits NSCLC cell invasion and metastasis possibly through targeted inhibition of CCL18/ STAT3 signaling pathway and EMT process.
Insights
Omega-3 fatty acids, specifically DHA, inhibit non-small cell lung cancer (NSCLC) metastasis by downregulating CCL18 expression and the STAT3 pathway. This finding offers a potential therapeutic strategy for lung cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Omega-3 fatty acids show antitumor potential, but mechanisms in lung cancer metastasis are unclear.
- Chemokine ligand 18 (CCL18) expression correlates with non-small cell lung cancer (NSCLC) migration and metastasis.
- Investigating omega-3's role in regulating CCL18 is crucial for understanding lung cancer progression.
Purpose of the Study:
- To determine if omega-3 fatty acids inhibit NSCLC invasion and metastasis by regulating CCL18 expression.
- To elucidate the molecular mechanisms underlying omega-3's anti-metastatic effects in NSCLC.
- To explore the relationship between CCL18, STAT3 signaling, and epithelial-mesenchymal transition (EMT) in NSCLC.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) and Western blotting to assess gene and protein expression.
- Scratch wound healing and Transwell assays to evaluate cell migration and invasion.
- Investigated the effects of docosahexaenoic acid (DHA) and CCL18 overexpression on NSCLC cell behavior and signaling pathways.
Main Results:
- CCL18 levels positively correlate with NSCLC metastatic potential.
- DHA significantly inhibited NSCLC cell invasion and metastasis.
- DHA downregulated metastasis-related genes, EMT markers, and the p-STAT3 signaling pathway.
- CCL18 overexpression reversed DHA's inhibitory effects, restoring metastatic gene expression and cell invasion.
Conclusions:
- Docosahexaenoic acid (DHA), an omega-3 fatty acid, inhibits NSCLC invasion and metastasis.
- DHA likely exerts its effects by downregulating CCL18 expression and inhibiting the STAT3 signaling pathway and EMT.
- Targeting the CCL18/STAT3 pathway presents a potential therapeutic strategy for managing NSCLC metastasis.
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