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Distinct in vivo expression patterns of survivin splice variants in renal cell carcinomas

Csaba Mahotka1, Thomas Krieg, Andreas Krieg

  • 1Institute of Pathology, Heinrich Heine-University, Duesseldorf, Germany.

Insights

This study analyzed survivin splice variants in renal cell carcinoma (RCC). Survivin-2B and survivin-Delta Ex3 are expressed in RCC, with survivin-2B decreasing in late stages, suggesting a role in tumor progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Oncology

Background:

  • Survivin, an inhibitor of apoptosis protein (IAP), promotes tumor cell survival.
  • Two novel splice variants, survivin-2B and survivin-Delta Ex3, exhibit different antiapoptotic properties.
  • Survivin-2B may antagonize the antiapoptotic effects of survivin and survivin-Delta Ex3.

Purpose of the Study:

  • To investigate the in vivo expression of survivin splice variants in human renal cell carcinoma (RCC).
  • To determine the correlation between survivin variant expression and RCC progression and clinical behavior.

Main Methods:

  • Quantitative reverse transcriptase polymerase chain reaction (RT-PCR) was used.
  • Expression levels of survivin, survivin-2B, and survivin-Delta Ex3 were analyzed in 57 RCC samples.
  • Comparison of expression between different RCC stages and subtypes.

Main Results:

  • All analyzed RCCs expressed survivin-Delta Ex3, survivin-2B, and survivin, with survivin being the dominant transcript.
  • No significant changes in survivin and survivin-Delta Ex3 expression were observed between early/intermediate and late stages of clear cell RCC.
  • A significant decrease in the mRNA ratio of survivin-2B to survivin was noted in late-stage clear cell RCC (p = 0.036).
  • Chromophilic/papillary RCCs did not exhibit significantly lower expression of survivin and survivin-Delta Ex3 compared to stage-matched clear cell RCCs.

Conclusions:

  • This study provides the first in vivo analysis of functionally distinct survivin splice variants in human RCC.
  • The findings suggest a potential role for survivin splice variants in the progression and clinical characteristics of RCC.
  • Survivin-2B's decreasing expression in advanced RCC warrants further investigation into its role as a potential tumor suppressor or antagonist.

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