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Characterisation of the Morphological, Functional and Molecular Changes in Sunitinib-Resistant Renal Cell Carcinoma

Hossam Kamli1,2, Gobe C Glenda1,3, Li Li4

  • 1Translational Research Institute, University of Queensland Princess Alexandra Hospital Kidney Disease Research Collaborative , Brisbane, Queensland, Australia.

Journal of Kidney Cancer and VHL
|August 16, 2018
PubMed

Insights

Developing sunitinib resistance in renal cell carcinoma (RCC) cells revealed significant cellular hypertrophy and increased interleukin-6 (IL-6). These changes may drive resistance via angiogenesis or altered apoptosis pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Sunitinib resistance is a significant clinical challenge in renal cell carcinoma (RCC) treatment.
  • Comprehensive characterization of morphological, functional, and molecular changes in resistant RCC cells is lacking.

Purpose of the Study:

  • To develop and characterize sunitinib resistance in human RCC cell lines.
  • To investigate the morphological, functional, and gene expression changes associated with sunitinib resistance.

Main Methods:

  • Developed sunitinib resistance in four human RCC cell lines (786-0, Caki-1, Caki-2, SN12K1) through chronic exposure.
  • Assessed cell proliferation, morphology, transmigration, and gene expression of IL-6, IL-8, VEGF, Bcl-2, and Bax.

Main Results:

  • No significant differences in growth rate or transmigration were observed between parental and resistant cells.
  • Sunitinib-resistant cells exhibited significant cellular and nuclear hypertrophy.
  • Increased IL-6 was observed in all resistant cell lines; IL-8 and VEGF showed varied changes, and the Bcl2/Bax ratio was altered, suggesting shifts in apoptosis regulation.

Conclusions:

  • Sunitinib resistance in RCC is associated with cellular hypertrophy and increased IL-6.
  • Elevated IL-6 may contribute to resistance by promoting VEGF-mediated angiogenesis or favoring anti-apoptotic pathways.
  • These findings provide insights into the mechanisms of sunitinib resistance in RCC.
Keywords:
angiogenesisanti-apoptosisinterleukin-6renal cell carcinomasunitinib resistance

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