Jam3 promotes migration and suppresses apoptosis of renal carcinoma cell lines.

As a common type of renal cancer, renal cell carcinoma (RCC) has a high annual mortality rate. The incidence of RCC has been increasing in China and worldwide. A large number cases of RCC are diagnosed at late stages, often with local and/or systematic metastasis. Surgical resection of RCC is only suitable for a small number of patients with early stage tumors, and thus, novel therapeutic methods are required. Junctional adhesion molecule 3 (Jam3) is a member of the junctional adhesion molecule family, which has been linked to epithelial and cancer cell proliferation. The present study investigated whether the Jam3 gene affected RCC growth via proliferation and apoptosis. The expression and biological function of Jam3 in renal carcinoma cells was investigated. The mRNA and protein levels of Jam3 were examined by reverse transcription‑polymerase chain reaction and western blot analyses. The role of Jam3 in the migration and apoptosis of renal carcinoma cells was determined using small interfering RNA, wound‑healing assays, flow cytometry, and cell migration assays. In the cell migration assays, E‑cadherin, N‑cadherin, integrin β1, and matrix metalloproteinase (MMP)‑2 proteins were detected by western blot analysis. It was shown that the expression of Jam3 was significantly elevated in human renal carcinoma cells compared with that in renal tubular epithelial cells. The knockdown of Jam3 inhibited renal carcinoma cell migration and promoted renal carcinoma cell apoptosis. It also increased the protein levels of E‑cadherin and reduced the protein levels of N‑cadherin, integrin β1 and MMP‑2. The inhibition of Jam3 promoted migration and suppressed apoptosis of renal carcinoma cells via regulation of the expression of E‑cadherin, N‑cadherin, integrin β1 and MMP‑2. Therefore, Jam3 was suggested as a novel target gene for the diagnosis and treatment of RCC.