ArticleArchives of pharmacal research2022
STAT3 mediates RCP-induced cancer cell invasion through the NF-κB/Slug/MT1-MMP signaling cascade.
Article in Archives of pharmacal research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 10 citations in OpenAlex.
- Matrix Metalloproteinase 14 in Corneal Neovascularization.International journal of molecular sciences · 2026Review
- Lathyrol affects the expression of AR and PSA and inhibits the malignant behavior of RCC cells.Open medicine (Warsaw, Poland) · 2025Article
- Rab25 suppresses colon cancer cell invasion through upregulating claudin‑7 expression.Oncology reports · 2024Article
- Macrophages in tumor cell migration and metastasis.Frontiers in immunology · 2024Review
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Rab coupling protein (RCP) has been known to induce cancer invasion and metastasis, and STAT3 is one of major oncogenic factors. In the present study, we identify the critical role of STAT3 in RCP-induced cancer cell invasion. Immunohistochemical data of ovarian cancer tissues presented that levels of RCP expression are closely correlated with those of phospho-STAT3 (p-STAT3). In addition, ovarian cancer patients with high expression of both RCP and p-STAT3 had significantly lower progress-free and overall survival rates compared to those with low either RCP or p-STAT3 expression. Mechanistically, RCP induced STAT3 phosphorylation in both ovarian and breast cancer cells. Silencing or pharmacological inhibition of STAT3 significantly inhibited RCP-induced cancer cell invasion. In addition, we provide evidence that the β1 integrin/EGFR axis is important for RCP-induced STAT3 phosphorylation. Furthermore, STAT3 activated NF-κB for Slug expression that in turn upregulated MT1-MMP expression for cancer cell invasion. Collectively, our present data demonstrate that STAT3 is located downstream of the β1 integrin/EGFR axis and induces Slug and MT1-MMP expression for cancer cell invasion.
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