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Polycystin-1 affects cancer cell behaviour and interacts with mTOR and Jak signalling pathways in cancer cell lines

Kostas A Papavassiliou1, Ilianna Zoi2, Antonios N Gargalionis3

  • 1Department of Physiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

Journal of Cellular and Molecular Medicine
|June 29, 2019
PubMed

Insights

Polycystin-1 (PC1), linked to Polycystic Kidney Disease, impacts cancer cell behavior. This study reveals PC1

Area of Science:

  • Oncology and Genetics
  • Molecular Biology
  • Cellular Biology

Background:

  • Polycystic Kidney Disease (PKD) shares cellular defects with cancer, including uncontrolled proliferation and apoptosis.
  • Mutations in PKD1 and PKD2 genes cause PKD, affecting polycystin-1 (PC1) and polycystin-2 (PC2) proteins.
  • PC1 regulates signaling pathways (e.g., Jak/STAT, mTOR, Wnt) crucial for cancer cell malignancy.

Purpose of the Study:

  • To investigate the role of polycystin-1 (PC1) in the biology of various cancer cell lines.
  • To explore the molecular relationship between polycystins and cancer development.
  • To determine PC1's impact on cell proliferation, migration, and key signaling pathways in cancer.

Main Methods:

  • In vitro investigation of PC1 function in glioblastoma (GOS3), prostate (PC3), breast (MCF7), lung (A549), and colorectal (HT29) cancer cell lines.
  • Assessing the effects of PC1 on cell proliferation and migration.
  • Analyzing PC1's interaction with mTOR and Jak signaling pathways.

Main Results:

  • PC1 differentially modulated cell migration: promoting it in GOS3 cells and suppressing it in A549 cells.
  • PC1's effect on cell proliferation varied: enhancing it in GOS3 cells but inhibiting it in MCF7, A549, and HT29 cells.
  • PC1 influenced signaling pathways, up-regulating mTOR and down-regulating Jak in GOS3 cells, and up-regulating mTOR in PC3 and HT29 cells.

Conclusions:

  • Polycystin-1 (PC1) plays a complex role in cancer, modulating cell proliferation and migration.
  • PC1 interacts with critical cancer signaling pathways like mTOR and Jak.
  • Further understanding of polycystin-cancer interactions may reveal novel therapeutic targets.
Keywords:
Jak signallingPC1cancercell migrationcell proliferationmTOR signallingpolycystins

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