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Serotonin's Role in Inflammatory Signaling Pathway Modulation for Colon Cancer Suppression.

Supreeta Maheshwarla Saravanan1, Lavanya Prathap1, Jabir Padathpeedika Khalid2

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Serotonin effectively inhibits growth and downregulates key inflammatory and cancer markers in KB cells. This study highlights serotonin

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adjuvant chemotherapyanti-inflammatory activityanti-inflammatory effectcancer inhibitioncolon cancerintermediate riskmismatch repairserotonin

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Area of Science:

  • Oncology
  • Neuroscience
  • Molecular Biology

Background:

  • Serotonin and dopamine regulate neurons, with potential in anti-inflammatory and chemotherapeutic research.
  • The study focuses on serotonin's anti-inflammatory and anticancer effects in HeLa (KB) cells.

Purpose of the Study:

  • Investigate serotonin's role in suppressing inflammation and its anticancer potential in KB cells.
  • Analyze molecular mechanisms of serotonin's action, including its interaction with Interleukin-6.

Main Methods:

  • In vitro and in silico analysis of serotonin's effects on KB cells.
  • Real-time RT-PCR to assess B-cell leukemia/lymphoma 2 protein (BCl-2), tumor necrosis factor-alpha (TNF-α), and Interleukin-6 (IL-6) expression.
  • Molecular docking using Schrodinger suites to analyze serotonin binding with human Interleukin-6.

Main Results:

  • Serotonin demonstrated significant growth inhibition in KB cells (IC50: 225±3.1µg/ml).
  • Downregulation of BCl-2, TNF-α, and IL-6 expression observed.
  • Molecular docking revealed efficient binding of serotonin to human Interleukin-6 (docking score: -5.65 kcal/mol).
  • Serotonin blocked NF-κB pathways in KB cells.

Conclusions:

  • Serotonin exhibits significant anticancer potential by blocking NF-κB pathways in KB cells.
  • Findings suggest serotonin as a promising therapeutic agent for colon cancer.
  • The study provides insights into serotonin's molecular interactions for potential clinical applications.