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Vanadocene dichloride induces apoptosis in HeLa cells through depolymerization of microtubules and inhibition of Eg5

Susobhan Mahanty1, Darpan Raghav1, Krishnan Rathinasamy2

  • 1School of Biotechnology, National Institute of Technology Calicut, Calicut, Kerala, 673601, India.

Journal of Biological Inorganic Chemistry : JBIC : a Publication of the Society of Biological Inorganic Chemistry
|May 31, 2021
PubMed

Insights

Vanadocene dichloride (VDC) inhibits cancer cell proliferation and induces apoptosis by disrupting microtubule dynamics and inhibiting Eg5 motor protein activity, revealing its anticancer mechanism.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Vanadocene dichloride (VDC) is a vanadium metallocene dihalide with demonstrated anticancer potential.
  • The precise mechanism of VDC's anticancer activity is not fully understood, with various targets and pathways proposed.

Purpose of the Study:

  • To elucidate the mechanism of action behind vanadocene dichloride's (VDC) antiproliferative and apoptotic effects on mammalian cancer cells.
  • To investigate VDC's impact on cellular processes, including mitochondrial function, microtubule dynamics, and key mitotic proteins.

Main Methods:

  • Assessed VDC's effects on cancer cell proliferation and apoptosis, including mitochondrial membrane potential and bcl2/bax expression.
  • Analyzed VDC's impact on microtubule polymerization, depolymerization, and microtubule-kinetochore interactions.
  • Investigated VDC's direct binding to tubulin and its effect on microtubule assembly dynamics.
  • Examined VDC's interaction with and inhibition of the mitotic kinesin Eg5 ATPase activity.

Main Results:

  • VDC inhibited cancer cell proliferation and induced apoptosis via mitochondrial pathways.
  • VDC caused microtubule depolymerization, mitotic arrest with monopolar spindles, and inhibited microtubule reassembly.
  • VDC bound to tubulin at a novel site, inhibiting microtubule polymerization and altering tubulin structure.
  • VDC inhibited the ATPase activity of the mitotic kinesin Eg5.

Conclusions:

  • VDC's anticancer activity stems from its disruption of microtubule assembly dynamics.
  • Inhibition of Eg5 kinesin ATPase activity by VDC contributes to its antimitotic effects.
  • Combined disruption of microtubule dynamics and Eg5 inhibition presents a plausible mechanism for VDC's antiproliferative and antimitotic actions.
Keywords:
4-(2-Pyridylazo)-resorcinolMetalloceneMitochondriaMitosisMitotic kinesin

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