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Background  Loss of PTEN is involved in tumor progression of several tumor entities including renal cell carcinoma (RCC). During the translation process PTEN generates a number of splice variants, including PTEN-Δ. We analyzed the impact of PTEN-Δ in RCC progression.    Methods  In specimens of RCC patients the expression of  PTEN-Δ  and  PTEN  was quantified. The PTEN expressing RCC cell line A498 and the PTEN deficient 786-O cell line were stably transfected with the  PTEN-Δ  or  PTEN  transcript. In Caki-1 cells that highly express PTEN-Δ, this isoform was knocked down by siRNA. Cell migration, adhesion, apoptosis and signaling pathways activities were consequently analyzed in vitro.    Results  Patients with a higher  PTEN-Δ  expression had a longer lymph node metastasis free and overall survival. In RCC specimens, the  PTEN-Δ  expression correlated with the  PTEN  expression. PTEN-Δ as well as PTEN induced a reduced migration when using extracellular matrix (ECM) compounds as chemotaxins. This effect was confirmed by knockdown of  PTEN-Δ , inducing an enhanced migration. Likewise a decreased adhesion on these ECM components could be shown in  PTEN-Δ  and  PTEN  transfected cells. The apoptosis rate was slightly increased by PTEN-Δ. In a phospho-kinase array and Western blot analyses a consequently reduced activity of AKT, p38 and JNK could be shown.    Conclusions  We could show that the PTEN splice variant PTEN-Δ acts similar to PTEN in a tumor suppressive manner, suggesting synergistic effects of the two isoforms. The impact of PTEN-Δ in context of tumor progression should thus be taken into account when generating new therapeutic options targeting PTEN signaling in RCC.    Electronic supplementary material  The online version of this article (10.1186/s12964-018-0247-9) contains supplementary material, which is available to authorized users.

In renal cell carcinoma the PTEN splice variant PTEN-Δ shows similar function as the tumor suppressor PTEN itself