The mammalian nitrilase (Nit) protein is a member of the nitrilase superfamily whose function remains to be characterized. We now show that the nitrilase family member 2 gene (NIT2) is ubiquitously expressed in multiple tissues and encodes protein mainly distributed in the cytosol. Ectopic expression of Nit2 in HeLa cells was found to inhibit cell growth through G2 arrest rather than by apoptosis. Consistent with this, proteomic and RT‐PCR analyses showed that Nit2 up‐regulated the protein and mRNA levels of 14‐3‐3σ, an inhibitor of both G2/M progression and protein kinase B (Akt)‐activated cell growth, and down‐regulated 14‐3‐3β, a potential oncogenic protein. Genotype analysis in four types of primary tumor tissues showed 12.5–38.5% allelic imbalance surrounding the NIT2 locus. The results demonstrated that NIT2 plays an important role in cell growth inhibition and links to human malignancies, suggesting that Nit2 may be a potential tumor suppressor candidate.

Anaplastic thyroid cancer (ATC) has a mean survival time of 6 months and accounts for 1–2% of all thyroid tumors. Understanding the underlying molecular mechanisms of carcinogenesis and progression in ATC would contribute to the identification of novel therapeutic targets. A previous study revealed that microRNA (miR)-599 was associated with tumor initiation and development in certain types of cancer. However, the specific functions and mechanisms of miR-599 in ATC are poorly understood. The objective of the present study was to identify its expression, function and molecular mechanism in ATC. The expression levels of miR-599 in 10 pairs of surgical specimens and human ATC cell lines were examined by reverse transcription-quantitative polymerase chain reaction. Function assays illustrated that miR-599 overexpression not only suppressed KAT-18 cell viability, proliferation and metastasis in vitro and decreased tumor growth in the tumor xenograft model but also induced cell apoptosis. Furthermore, T-cell intracellular antigen (TIA1), a tumor suppressor, was confirmed as a direct target of miR-599. It was demonstrated that TIA1 silencing rescued the inhibitory effect of migration and invasion induced by the overexpression of miR-599 in KAT-18 cells. In conclusion, the present study revealed that miR-599 inhibited ATC cell growth and metastasis via activation of TIA1. Therefore miR-599 may be a novel molecular therapeutic target for ATC.