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Genistein induces growth arrest and suppresses telomerase activity in brain tumor cells
Aik Kia Khaw1, Jacklyn Wei Yan Yong, Guruprasad Kalthur
1Department of Physiology, Genome Stability Laboratory, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Republic of Singapore.
Abstract:
Genistein, a soy isoflavone, has been reported to exhibit multiple effects, such as inducing cell cycle arrest, triggering apoptosis, inhibiting the activation of NF(K) B and inactivating several signaling cascades in human cancer cells. In vivo studies demonstrating antiangiogenesis and antimetastatic effects of genistein have also been reported. Here, we demonstrate that genistein inhibits the growth of glioblastoma multiforme and medulloblastoma cells with different TP53 mutations and radio-responses by arresting the cells at G2/M phase of the cell cycle. The cell cycle arrest was found to be independent of DNA damage and such an arrest was sustainable for at least 10 days even after drug removal. Annexin V staining revealed absence of apoptotic or necrotic cell populations after genistein treatment. This supports the observation that genistein induces insignificant DNA damage and indicates that the cell cycle arrest triggered does not lead to cell death. Gene and protein expression studies reveal similar changes in the same pathways following treatment in the cell types tested. Genistein was also able to inhibit telomerase activity resulting in telomere shortening. Thus, we demonstrate, for the first time, that genistein induces growth arrest in association with telomerase inhibition in brain tumor cells via the suppression of TR- and TERT mRNA. By elucidating the mechanisms of anticancer effects after genistein treatment in brain tumor cells, there will be a premise for the incorporation of genistein dietary sources to complement radiotherapy in brain tumor patients.
Insights
Genistein, a soy isoflavone, halts brain tumor cell growth by arresting the cell cycle without causing DNA damage. This study shows genistein inhibits telomerase, offering a potential dietary complement to radiotherapy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Genistein, a soy isoflavone, exhibits anticancer properties including cell cycle arrest and apoptosis induction in various cancer cells.
- Previous studies suggest genistein has antiangiogenic and antimetastatic effects in vivo.
- Glioblastoma multiforme and medulloblastoma are aggressive brain tumors with limited treatment options.
Purpose of the Study:
- To investigate the effects of genistein on glioblastoma multiforme and medulloblastoma cell growth.
- To elucidate the underlying mechanisms of genistein's anticancer activity in brain tumors.
- To explore the potential of genistein as a complementary therapy for brain tumors.
Main Methods:
- Genistein treatment of glioblastoma and medulloblastoma cell lines with varying TP53 mutations and radio-responses.
- Cell cycle analysis using flow cytometry to assess G2/M phase arrest.
- Annexin V staining to evaluate apoptosis and necrosis.
- Gene and protein expression analysis to identify affected pathways.
- Telomerase activity and telomere length assays.
Main Results:
- Genistein inhibited the growth of both glioblastoma and medulloblastoma cells by inducing G2/M cell cycle arrest.
- The cell cycle arrest was sustained for at least 10 days and was independent of DNA damage, with no significant apoptosis or necrosis observed.
- Genistein suppressed telomerase activity, leading to telomere shortening through the downregulation of TR- and TERT mRNA.
- Similar pathway alterations were observed across tested cell types following genistein treatment.
Conclusions:
- Genistein effectively induces growth arrest in brain tumor cells, specifically glioblastoma and medulloblastoma, via G2/M cell cycle arrest.
- Genistein's mechanism involves telomerase inhibition and telomere shortening, independent of DNA damage induction or apoptosis.
- These findings provide a basis for considering genistein-rich dietary sources as a complementary strategy alongside radiotherapy for brain tumor patients.
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