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Tetrahydroisoquinoline reduces angiogenesis by interacting myeloma cells with HUVECs mediated by extracellular

Ahmad Kooshari1, Fahimeh Shahriyary1, Minoo Shahidi2

  • 1Department of Hematology and Blood Banking, Faculty of Allied Medicine, Iran University of Medical Sciences, Hemmat Highway, Tehran, 14155-5983, Iran.

Medical Oncology (Northwood, London, England)
|August 5, 2024
PubMed

Insights

Tetrahydroisoquinoline (THIQ)-treated multiple myeloma (MM) extracellular vesicles (EVs) inhibit blood vessel formation in endothelial cells. This suggests THIQ-modified MM-EVs may offer a novel therapeutic strategy for MM by reducing angiogenesis.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Multiple myeloma (MM) is a cancer of plasma cells, where angiogenesis plays a crucial role in disease progression.
  • Extracellular vesicles (EVs) mediate cell-to-cell communication and are implicated in angiogenesis.
  • Tetrahydroisoquinoline (THIQ) is a bioactive compound with potential therapeutic applications.

Purpose of the Study:

  • To investigate the effects of MM-derived EVs, treated with THIQ, on endothelial cell (EC) angiogenesis.
  • To determine if THIQ-modified MM-EVs can alter gene and protein expression related to angiogenesis in ECs.

Main Methods:

  • Multiple myeloma cells (U266) were treated with THIQ, and subsequently, MM-EVs were isolated.
  • MM-EVs were co-cultured with human umbilical vein endothelial cells (HUVECs) to assess transmigration, gene/protein expression (RT-PCR, ELISA), proliferation, and migration (tube formation, scratch wound healing).
  • EV transmigration was quantified using flow cytometry.

Main Results:

  • THIQ-treated MM-EVs were internalized by HUVECs.
  • Internalization of THIQ-treated MM-EVs led to decreased expression of angiogenic markers CD34, VEGFR2, and IL-6 at both mRNA and protein levels.
  • THIQ-treated MM-EVs significantly inhibited HUVEC proliferation and migration, as evidenced by reduced tube formation and impaired scratch wound healing.

Conclusions:

  • MM-EVs derived from THIQ-treated myeloma cells exhibit anti-angiogenic properties.
  • The anti-angiogenic effect is mediated by the internalization of THIQ-treated MM-EVs into HUVECs, leading to reduced expression of key angiogenic factors.
  • THIQ-modified MM-EVs demonstrate potential as a novel therapeutic approach to inhibit angiogenesis in multiple myeloma.
Keywords:
AngiogenesisExtracellular vesicles (EVs)IL-6Multiple myeloma (MM)Tetrahydroisoquinoline (THIQ)Vascular endothelial growth factor receptor 2 (VEGFR-2)

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