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The  SEMA3B  gene is located in the 3p21.3 LUCA region, which is frequently affected in different types of cancer. The objective of our study was to expand our knowledge of the  SEMA3B  gene as a tumor suppressor and the mechanisms of its inactivation. In this study, several experimental approaches were used: tumor growth analyses and apoptosis assays  in vitro  and in SCID mice, expression and methylation assays and other. With the use of the small cell lung cancer cell line U2020 we confirmed the function of  SEMA3B  as a tumor suppressor, and showed that the suppression can be realized through the induction of apoptosis and, possibly, associated with the inhibition of angiogenesis. In addition, for the first time, high methylation frequencies have been observed in both intronic (32-39%) and promoter (44-52%) CpG-islands in 38 non-small cell lung carcinomas, including 16 squamous cell carcinomas (SCC) and 22 adenocarcinomas (ADC), and in 83 clear cell renal cell carcinomas (ccRCC). Correlations between the methylation frequencies of the promoter and the intronic CpG-islands of  SEMA3B  with tumor stage and grade have been revealed for SCC, ADC and ccRCC. The association between the decrease of the  SEMA3B  mRNA level and hypermethylation of the promoter and the intronic CpG-islands has been estimated in renal primary tumors ( P  < 0.01). Using qPCR, we observed on the average 10- and 14-fold decrease of the  SEMA3B  mRNA level in SCC and ADC, respectively, and a 4-fold decrease in ccRCC. The frequency of this effect was high in both lung (92-95%) and renal (84%) tumor samples. Moreover, we showed a clear difference ( P  < 0.05) of the  SEMA3B  relative mRNA levels in ADC with and without lymph node metastases. We conclude that aberrant expression and methylation of  SEMA3B  could be suggested as markers of lung and renal cancer progression.

Tumor Suppressor Function of the SEMA3B Gene in Human Lung and Renal Cancers