Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 14, Issue 5, Pages 8801-8817Publisher
MDPI
DOI: 10.3390/ijms14058801
Keywords
oral cancer; caffeic acid phenethyl ester; TW2.6; cell proliferation; cell cycle; Akt; Akt1; Akt2; phospho-Akt Ser473; phospho-Akt Thr 308; FOXO1; FOXO3a; phospho-FOXO1 Thr24; phospho-FoxO3a Thr32; NF-kappa B; phospho-NF-kappa B Ser536; Rb; phospho-Rb Ser807/811; Skp2; cyclin D1; p27; 5-fluorouracil
Funding
- National Health Research Institutes, NHRI [CS-101-PP-14, CS-102-PP-14]
- National Science Council, NSC in Taiwan [NSC 99-2320-B-400-015-MY3, NSC 101-2325-B-400-014]
- Department of Health, DOH in Taiwan [DOH101-TD-C-111-004, DOH102-TD-C-111-004]
- Taiwan Tech Trek intern fellowship from Taiwan (NSC)
- protein chemistry Micro-Western Array core facility and cell sorter core facility of NHRI
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Caffeic acid phenethyl ester (CAPE) is a bioactive component extracted from honeybee hive propolis. Our observations indicated that CAPE treatment suppressed cell proliferation and colony formation of TW2.6 human oral squamous cell carcinoma (OSCC) cells dose-dependently. CAPE treatment decreased G1 phase cell population, increased G2/M phase cell population, and induced apoptosis in TW2.6 cells. Treatment with CAPE decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3 beta, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-kappa B, phospho-NF-kappa B Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27(Kip). Overexpression of Akt1 or Akt2 in TW2.6 cells rescued growth inhibition caused by CAPE treatment. Co-treating TW2.6 cells with CAPE and 5-fluorouracil, a commonly used chemotherapeutic drug for oral cancers, exhibited additive cell proliferation inhibition. Our study suggested that administration of CAPE is a potential adjuvant therapy for patients with OSCC oral cancer.
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