Open AccessHIPK2 inhibits cell metastasis and improves chemosensitivity in esophageal squamous cell carcinoma
Author(s) -
Zhen Zhang,
Penghaο Wen,
Fangfang Li,
Chuanshan Yao,
Tongfu Wang,
Bing Liang,
Qingle Yang,
Lei Ma,
Liang He
Publication year - 2017
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2017.5468
Subject(s) - oncogene , esophageal squamous cell carcinoma , cancer research , oncology , cell cycle , molecular medicine , metastasis , cell , medicine , basal cell , carcinoma , biology , cancer , genetics
Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive and lethal malignancies worldwide. At present, the underlying mechanisms of ESCC development and progression are poorly understood. Previous studies have demonstrated that homeodomain-interacting protein kinase-2 (HIPK2) serves an important role in cancer biology, particularly in proliferation and metastasis. However, the role of HIPK2 in ESCC cells remains unclear. In the current study, the expression of HIPK2 in ESCC specimens, adjacent non-cancerous tissues and cell lines was assessed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The effects of HIPK2 on cell metastasis, epithelial-mesenchymal transition (EMT) and proliferation were studied using a Transwell assay, RT-qPCR and a Cell Counting Kit-8 assay, respectively. The results indicated that HIPK2 expression was downregulated in ESCC specimens and cell lines, and HIPK2 expression was associated with tumor invasion and lymph node metastasis. Functional studies demonstrated that HIPK2 overexpression inhibited cell metastasis and EMT. Furthermore, HIPK2 overexpression suppressed cell viability during cisplatin treatment. These results suggest that HIPK2 serves an important role in regulating metastasis and the chemosensitivity of ESCC cells, implicating the potential application of HIPK2 in ESCC therapy.