Isobavachalcone inhibits the proliferation and invasion of tongue squamous cell carcinoma cells

Shi,Yi; Wu,Wei‑Zhong; Huo,An; Zhou,Wei; Jin,Xiao‑Hong

doi:10.3892/ol.2017.6517

Isobavachalcone inhibits the proliferation and invasion of tongue squamous cell carcinoma cells

Authors:
- Yi Shi
- Wei‑Zhong Wu
- An Huo
- Wei Zhou
- Xiao‑Hong Jin
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Affiliations: Department of Stomatology, Danyang People's Hospital of Jiangsu, Danyang, Jiangsu 212300, P.R. China, Department of Oncology, Yunyang People's Hospital of Danyang, Danyang, Jiangsu 212300, P.R. China
Published online on: July 4, 2017 https://doi.org/10.3892/ol.2017.6517
Pages: 2852-2858
Copyright: © Shi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Isobavachalcone (2',4',4‑trihydroxy‑3'‑[3'‑methylbut‑3'‑ethyl] chalcone or IBC) exhibits anticancer activities in a number of types of cancer cell. However, its role in tongue squamous cell carcinoma (TSCC) cells remains unclear. The aim of the present study was to investigate the biological effect of IBC in TSCC Tca8113 cells. The function of IBC on Tca8113 cell apoptosis and apoptosis‑associated signaling pathways was determined using an MTT assay, morphological staining, annexin V‑propidium iodide (PI) staining and Western blot analysis. The effects of IBC on Tca8113 cell migration, invasion and relative protein expression were confirmed using wound healing analysis, Transwell invasion analysis and Western blot analysis, respectively. The results of the MTT assay and annexin V‑PI staining indicated that IBC is able to significantly inhibit proliferation and induce apoptosis of Tca8113 cells in vitro. IBC treatment resulted in typical apoptotic morphology of nuclear fragmentation and apoptotic bodies in Tca8113 cells. Western blot analysis further demonstrated that IBC caused downregulation of the expression of B‑cell lymphoma 2 (Bcl‑2) protein, upregulation of the expression of Bcl‑2‑associated X protein (Bax), activation of caspases, and dephosphorylation of protein kinase B (Akt) and extracellular‑signal‑regulated kinase (ERK) proteins in a concentration‑ and time‑dependent manner. The results of the present study suggest that IBC induces apoptosis in Tca8113 cells and that the induction may be associated with the activation of Bcl‑2, Bax and caspase‑3, and the inactivation of Akt and ERK. Furthermore, IBC inhibited migration and invasion of Tca8113 cells in vitro by downregulating matrix metalloproteinase (MMP)‑2 and MMP‑9 protein expression. The results of the present study indicate that IBC may be a potential anticancer drug for the treatment of TSCC.

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