Nasopharyngeal carcinoma (NPC) has a highly increased incidence rate (20/100,000) in Southern regions of China, while being rare in the rest of the world. NPC is a malignant type of
cancer due to its high occurrence rate of
metastasis; however,
biomarkers for effective diagnosis and treatment are yet to be identified.
Annexin A1 is a glucocorticoid‑regulated member of a large superfamily of
calcium and phospholipid‑binding
proteins and has been shown to have important roles in
tumor development and progression, and was demonstrated to be a prognostic
biomarker for
head and neck cancer types. A previous study by our group showed that
Annexin A1 was decreased in NPC tissue as compared with normal adjacent tissue. To investigate whether
Annexin A1 is a potential
biomarker for NPC, the present study assessed the effect of the
Annexin A1 on the
biological behavior (i.e., invasion and
metastasis) of the highly metastatic NPC cell line 5‑8F and the non‑metastatic NPC cell line 6‑10B. The expression levels of
Annexin A1 in the above two cell lines were determined by western blot analysis. Next, the recombinant plasmid pEGFP‑C1‑Annexin A1 and the small interfering (si)
RNA plasmid pRNAT‑U6.1‑Annexin A1 were used and stably transfected into 5‑8F and 6‑10B cells, respectively. These established recombinant cell lines were then used to study the up- and downregulation of
Annexin A1, respectively. The correlation of
Annexin A1 expression levels with the
biological behavior of NPC cell lines was analyzed using a cell proliferation assay, flow cytometry, soft
agar colony formation assay, as well as Transwell invasion and migration assays. The results demonstrated that upregulation of
Annexin A1 suppressed the proliferation, invasion and migration of NPC cells, while downregulation of
Annexin A1 promoted the proliferation, invasion and migration of NPC cells. These findings suggested that
Annexin A1 may be a potential
biomarker for the development and prognosis of NPC, and its dysregulation may have an important role in its underlying pathogenesis.