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The function of FAK/CCDC80/E-cadherin pathway in the regulation of B16F10 cell migration

Guoshun Pei1, Yan Lan1, Weijie Lu1

  • 1The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210046, P.R. China.

Oncology Letters
|September 15, 2018
PubMed

Insights

Focal adhesion kinase (FAK) regulates melanoma cell migration by affecting coiled-coil domain containing 80 (CCDC80) and E-cadherin expression. FAK knockdown increases CCDC80 and E-cadherin, inhibiting cell migration, suggesting FAK

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Focal adhesion kinase (FAK) is a key regulator in cancer development and progression.
  • The precise role of FAK in controlling cancer cell migration, particularly in melanoma, requires further elucidation.
  • Understanding FAK's regulatory mechanisms is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To investigate the mechanism by which FAK regulates melanoma cell migration.
  • To determine the relationship between FAK, coiled-coil domain containing 80 (CCDC80), and E-cadherin in melanoma cells.
  • To explore the potential of targeting FAK/CCDC80 pathway for melanoma treatment.

Main Methods:

  • Gene chip analysis to assess gene expression changes upon FAK knockdown in B16F10 melanoma cells.
  • Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting to analyze CCDC80 and E-cadherin expression.
  • Wound healing and transwell assays to evaluate the impact of FAK and CCDC80 on melanoma cell migration.

Main Results:

  • FAK knockdown led to increased expression of CCDC80 and E-cadherin in B16F10 cells.
  • CCDC80 overexpression elevated E-cadherin expression, while CCDC80 downregulation promoted cell migration.
  • Clinical data indicated elevated FAK mRNA and decreased CCDC80/E-cadherin mRNA in melanoma patients.
  • Upregulation of CCDC80 inhibited B16F10 cell migration, whereas its downregulation promoted migration.

Conclusions:

  • FAK-mediated regulation of melanoma cell migration is potentially achieved through modulation of CCDC80 expression.
  • CCDC80 acts as a suppressor of melanoma cell migration, partly by influencing E-cadherin levels.
  • Targeting the FAK-CCDC80 axis may represent a novel therapeutic strategy for melanoma.
Keywords:
coiled-coil domain containing 80epithelial cadherinfocal adhesion kinasemelanomamigration

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