ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

Abstract

Abstract. Annexin A1 (ANXA1) acts either as a tumor suppressor or an oncogene in different tumor types. Several clinical studies revealed that the expression of ANXA1 is associated with the pathologic differentiation grade in oral squamous cell carcinoma (OSCC) patients. However, the direct function of ANXA1 in OSCC progression has remained to be fully clarified. The present study was designed to investigate the role of ANXA1 in OSCC cell proliferation and invasion in vitro. Furthermore, whether ANXA1 was involved in transforming growth factor β1 (TGFβ1)/epidermal growth factor (EGF)-induced epithelial-mesenchymal transition (EMT) in OSCC was explored. Tca-8113 and SCC-9 cells were transfected with ANXA1-pcDNA3.1 plasmid to overexpress ANXA1. Subsequently, cell proliferation and invasion were examined using MTT and Transwell-Matrigel invasion assays. TGFβ1 and EGF were used to induce EMT in Tca-8113 and SCC-9 cells, and the expression of epithelial (E)-cadherin, neural (N)-cadherin and vimentin was determined by western blot analysis. The results demonstrated that ANXA1 overexpression induced a significant decrease of cell growth and invasiveness in Tca-8113 and SCC-9 cells. The expression of E-cadherin was significantly increased, while the expression of vimentin and N-cadherin was significantly decreased in ANXA1-overexpressing Tca-8113 and SCC-9 cells. ANXA1 expression was significantly decreased in TGFβ1/EGF-treated cells. Furthermore TGFβ1/EGF-induced EMT in OSCC cell lines was attenuated by ANXA1 overexpression. In conclusion, to the best of our knowledge, the present study was the first to evidence that ANXA1 inhibits OSCC cell proliferation and invasion in vitro. TGFβ1/EGF-induced EMT was reversed by ANXA1 in OSCC. ANXA1 was suggested to be a potential marker for OSCC as well as a novel treatment.

Biological and physical approaches on the role of piplartine (piperlongumine) in cancer

“…Previous studies from our group 52 have already shown that the peptide induces cell proliferation in HUVECs, both under basal conditions and after stimulation by VEGF. Other studies using inflammation and tumor models evidenced that ANXA1 may stimulate proliferation and migration 53 or even inhibit proliferation 54 , most likely depending on the context of the experiment, cell type or tissue. Treatment of HUVECs with PL, alone or together with Ac 2-26 , also showed a low effect on cell viability.…”

Prognostic Values of Long Noncoding RNA linc00152 in Various Carcinomas: An Updated Systematic Review and Meta-Analysis

“…Moreover, the GO and KEGG were carried out. The result of our analysis showed that LGALS1, ANXA1, and ANXA2, which have an important roles in multiple tumors including clear cell renal cell carcinoma , pancreatic cancer , acute lymphoblastic leukemia , breast cancer , and oral squamous cell carcinoma , were significantly related to linc00152 gene expression ( P < 4.12 × 10 −60 ). Following this, we performed the GO and KEGG pathway analysis, and the results showed that linc00152 was significantly related to negative regulation of apoptotic processes.…”

iTRAQ-based quantitative proteomic analysis of differentially expressed proteins in chemoresistant nasopharyngeal carcinoma

“…ANXA1, a member of the annexins superfamily, is a structurally related calcium-dependent phospholipid-binding protein that has a core domain shared by the annexins superfamily and an N-terminal domain that is responsible for its unique function. It participates in important cell processes such as cell signaling, cell differentiation and apoptosis through regulating bubble aggregation, inflammatory response and the activity of phospholipase A2.More and more evidence shows that,ANXA1 affects cell proliferation, invasion, epithelial-mesenchymal transition [79][80][81][82] and chemoresistance. 39,83,84 ANXA1 is a substrate for protease C and tyrosinase, and possesses multiple calcium-phosphorus binding sites.…”