ArticleScientific reports2016
p-Hydroxylcinnamaldehyde induces the differentiation of oesophageal carcinoma cells via the cAMP-RhoA-MAPK signalling pathway.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- A Novel Autophagy InhibitorResearch (Washington, D.C.) · 2026Article
- CMSP suppresses oral squamous cell carcinoma progression by targeting the JAK2/STAT3/c-Myc axis.Frontiers in oncology · 2025Article
- Momordicae Semen: A Review of Phytochemistry, Pharmacology, Toxicology, Herbal Processing, Clinical Applications, and Q-Markers Prediction.Drug design, development and therapy · 2025Review
- CMSP exerts anti-tumor effects on small cell lung cancer cells by inducing mitochondrial dysfunction and ferroptosis.Open medicine (Warsaw, Poland) · 2025Article
- Enhanced understanding of cinnamaldehyde's therapeutic potential in osteoarthritis through bioinformatics and mechanistic validation of its anti-apoptotic effect.Frontiers in medicine · 2024Article
- Article
- lncRNA Profiles Enable Prognosis Prediction and Subtyping for Esophageal Squamous Cell Carcinoma.Frontiers in cell and developmental biology · 2021Article
- Knockdown of FAM83D Enhances Radiosensitivity in Coordination with Irradiation by Inhibiting EMT via the Akt/GSK-3β/Snail Signaling Pathway in Human Esophageal Cancer Cells.OncoTargets and therapy · 2020Article
- ERK is a Pivotal Player of Chemo-Immune-Resistance in Cancer.International journal of molecular sciences · 2019Review
- ADAMTS8 targets ERK to suppress cell proliferation, invasion, and metastasis of hepatocellular carcinoma.OncoTargets and therapy · 2018Article
- BIN1 reverses PD-L1-mediated immune escape by inactivating the c-MYC and EGFR/MAPK signaling pathways in non-small cell lung cancer.Oncogene · 2017Article
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7 authors.
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Abstract
p-Hydroxylcinnamaldehyde (CMSP) has been identified as an inhibitor of the growth of various cancer cells. However, its function in oesophageal squamous cell carcinoma (ESCC) and the underlying mechanism remain unclear. The aim of the present study was to characterize the differentiation effects of CMSP, as well as its mechanism in the differentiation of ESCC Kyse30 and TE-13 cells. The function of CMSP in the viability, colony formation, migration and invasion of Kyse30 and TE-13 cells was determined by MTS, colony-formation, wound healing and transwell assays. Western blotting and pull-down assays were used to investigate the effect of CMSP on the expression level of malignant markers of ESCC, as well as the activity of MAPKs, RhoA and GTP-RhoA in Kyse30 and TE-13 cells. We found that CMSP could inhibit proliferation and migration and induce Kyse30 and TE-13 cell differentiation, characterized by dendrite-like outgrowth, decreased expression of tumour-associated antigens, as well as the decreased expression of malignant markers. Furthermore, increased cAMP, p-P38 and decreased activities of ERK, JNK and GTP-RhoA, were detected after treatment with CMSP. These results indicated that CMSP induced the differentiation of Kyse30 and TE-13 cells through mediating the cAMP-RhoA-MAPK axis, which might provide new potential strategies for ESCC treatment.
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