Abstract
Bcl-2 and Twist1 can be coactivated by hypoxia in hepatocellular carcinoma to promote tumor cell metastasis and vasculogenic mimicry, but their function in oral squamous cell carcinoma (OSCC) remains undefined. We employed a cohort of 82 cases of OSCC samples to examine the coexpression of Bcl-2 and Twist1 by immunohistochemistry and demonstrate the interaction between Bcl-2 and Twist1 by coimmunoprecipitation. Bcl-2 and Twist1 overexpression was associated with a poor pathological grade and tumor prognosis, and the two factors functions as a complex. Knocking down Bcl-2/Twist1 inhibited cell migration, decreased cell invasion and inversed cell epithelial-mesenchymal transition (EMT) procession. An animal model derived from the Tca8113 cell line was used to further validate the role of Bcl-2/Twist1 depletion in suppressing tumor EMT and growth. In conclusion, Bcl-2/Twist1 complex can be treated as a potential therapeutic target for OSCC.
Highlights
Oral squamous cell carcinoma (OSCC) is the most common pathological type of oral cancer, and is the major cancer type for head and neck carcinoma [1]
The expression levels of B-cell lymphoma-2 (Bcl-2), Twist1, E-cadherin, N-cadherin, Vimentin and matrix metalloproteina-2/9 (MMP-2/9) were significantly associated with lymph node metastasis (Table 2 and Figure 1A), and the differences in the pathologic grades were significant
Juan An et al [21] revealed that in breast cancer, constitutive Bcl-2 expression affects the expression of the genes that determine cellular behaviors, such as the loss of epithelial cellular marker E-cadherin and gain of mesenchymal N-cadherin
Summary
Oral squamous cell carcinoma (OSCC) is the most common pathological type of oral cancer, and is the major cancer type for head and neck carcinoma [1] It is characterized by local invasion and a high rate of cervical lymph nodes metastasis, which are the main factors contributing to poor prognosis. The epithelial-mesenchymal transition (EMT) has generally been considered as an important mechanism for tumor metastasis, which converts epithelial cells into a mesenchymal-like phenotype [2] This phenotypic switch including loss of cell contact, upregulation of N-cadherin, Vimentin, Snail, Slug, Twist and decreased expression of E-cadherin inversely is important for cell for cancer cells to migrate, invade and induce tumor dissemination from primary site to a secondary organ [3, 4]. Bcl-2 can bind to Twist and formation of the Bcl-2/Twist complex facilitates the nuclear transport of Twist and increase the tumor cell plasticity, metastasis, and vasculogenic mimicry
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