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Updated: Feb 28, 2026
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
The inhibitory effects of deep-sea water on doxorubicin‑induced epithelial-mesenchymal transition
So-Young Chun1, Soyoung Kim1, Kyung-Soo Nam1
1Department of Pharmacology, School of Medicine and Intractable Disease Research Center, Dongguk University, 123 Dongdae-ro, Gyeongju-si 38066, Republic of Korea.
Abstract:
It has been revealed that the induction of epithelial‑mesenchymal transition (EMT) is associated with drug resistance, leading to tumor recurrence and metastasis. Recent studies have shown that chemotherapeutic agents, besides their therapeutic effects, can induce EMT and enhance invasive and metastatic properties of tumor cells. Previously, we revealed that deep-sea water (DSW) exhibited antimetastatic effects in several human cancer cell lines. In the present study, we investigated the effects of DSW on doxorubicin-induced EMT in MCF-7 human breast cancer cells. When treated with doxorubicin, MCF-7 cells displayed characteristics of EMT, such as, mesenchymal markers (vimentin and fibronectin) and EMT-related transcription factors (Slug and Snail-1) in their RNA expression. However, DSW efficiently inhibited doxorubicin-induced EMT, revealing the decreased expression of vimentin, fibronectin, Slug and Snail-1. Moreover, treatment of MCF-7 cells with DSW significantly suppressed their increased migratory ability by doxorubicin as determined by wound-healing assay. We further demonstrated that the inhibitory effects of DSW on doxorubicin-induced EMT appeared to be mediated by inhibition of the ERK1/2, p38 MAPK and PI3K/AKT signaling pathways. Collectively, our data revealed that DSW has the potential to abolish undesired side-effects of doxorubicin by targeting EMT.
Insights
Deep-sea water (DSW) inhibits chemotherapy-induced epithelial-mesenchymal transition (EMT) in breast cancer cells. DSW reduces cancer cell migration and targets key signaling pathways, offering a potential strategy to mitigate doxorubicin
Area of Science:
- Oncology
- Molecular Biology
- Marine Biotechnology
Background:
- Epithelial-mesenchymal transition (EMT) is linked to drug resistance, tumor recurrence, and metastasis.
- Chemotherapeutic agents can paradoxically induce EMT, enhancing cancer cell invasion.
- Deep-sea water (DSW) has previously demonstrated antimetastatic effects.
Purpose of the Study:
- To investigate the effect of DSW on doxorubicin-induced EMT in MCF-7 human breast cancer cells.
- To determine if DSW can counteract the pro-metastatic effects of doxorubicin.
- To elucidate the signaling pathways involved in DSW's inhibitory action.
Main Methods:
- MCF-7 cells were treated with doxorubicin and DSW.
- RNA expression of mesenchymal markers (vimentin, fibronectin) and EMT transcription factors (Slug, Snail-1) was analyzed.
- Cell migration was assessed using a wound-healing assay.
- Key signaling pathways (ERK1/2, p38 MAPK, PI3K/AKT) were investigated.
Main Results:
- Doxorubicin treatment induced EMT markers and increased cell migration in MCF-7 cells.
- DSW significantly inhibited doxorubicin-induced EMT by decreasing vimentin, fibronectin, Slug, and Snail-1 expression.
- DSW suppressed doxorubicin-enhanced cell migration.
- DSW's inhibitory effects were mediated through the suppression of ERK1/2, p38 MAPK, and PI3K/AKT signaling pathways.
Conclusions:
- DSW effectively inhibits doxorubicin-induced EMT in breast cancer cells.
- DSW reduces cancer cell migration potentially by targeting EMT.
- DSW may mitigate adverse side effects of doxorubicin by targeting EMT and associated signaling pathways.
