ABSTRACT
Objective: To assess the expression of ajuba LIM protein (AJUBA) in oral squamous cell carcinoma (OSCC) and to determine its role in cell proliferation, migration, and invasion in OSCC. Methods: The expression of AJUBA at mRNA and protein levels in OSCC was determined by quantitative polymerase chain reaction (qPCR) and immunohistochemical approaches, respectively. This was fol-lowed by analysis of the correlations between AJUBA levels and clinicopathological features of OSCC. The effects of AJUBA on cell pro-liferation, migration, and invasion in OSCC were assessed by MTT, wound healing, and transwell migration assays, respectively. West-ern blot assays were performed to check for the potential regulation of the Snail/E-cadherin pathway by AJUBA. Results: The expres-sion of AJUBA was significantly higher in OSCC tissues compared to that in adjacent normal tissues and correlated with T stage, cell dif-ferentiation, lymph node metastasis, and recurrence in OSCC. Elevated AJUBA levels indicated poor prognosis in patients with OSCC. Depletion of AJUBA impaired cell proliferation, migration, and invasion abilities of OSCC cells. Data from Western blot assays showed that AJUBA facilitated the expression of Snail but inhibited that of E-cadherin. Conclusions: AJUBA is overexpressed in OSCC and may influence cell proliferation and invasion in OSCC by modulating the Snail/E-cadherin pathway.
ABSTRACT
Ajuba was found in cell connections, and the subsequent studies showed that it can shuttle between the nucleus and cytoplasm for signals transmission. Under normal physiological conditions, Ajuba promotes cell proliferation and differentiation by regulating cell cycle and participating in signaling pathways. In addition, Ajuba is closely related to the development of various tumors, such as breast cancer, colorectal cancer, head and neck squamous cell carcinoma, etc. However, Ajuba functions as an oncogene or a tumor suppressor gene in different tumors. In carcinomas, Ajuba can also promote tumor cell proliferation and promote tumor invasion and metastasis by regulating epithelial-mesenchymal transition. Some progress has been made in the development of small molecular inhibitors or targeted drugs for Ajuba, and there are considerable therapeutic prospects.