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Updated: Aug 8, 2026

Analysis of Cell Cycle Position in Mammalian Cells
Published on: January 21, 2012
Ki-67 as a marker for cell cycle regulation by interferon
D Lundblad1, G Landberg, G Roos
1Institute of Applied Cell and Molecular Biology, University of Umeå, Sweden.
Insights
Interferon (IFN) treatment reduced Ki-67 expression in some cancer cells but not others. Ki-67 antigen is not a reliable marker for monitoring clinical effects of IFN therapy.
Area of Science:
- Cell biology
- Immunology
- Oncology
Background:
- Interferon (IFN) is a crucial cytokine in immune response and cancer therapy.
- Ki-67 is a nuclear antigen commonly used as a marker for cell proliferation.
Purpose of the Study:
- To investigate the effect of interferon on Ki-67 expression in different cancer cell lines.
- To determine if Ki-67 can serve as a reliable biomarker for interferon treatment efficacy.
Main Methods:
- Treatment of IFN-sensitive (Daudi, 251 MG) and IFN-resistant (Namalwa) cell lines with interferon.
- Analysis of Ki-67 expression and cell cycle distribution using flow cytometry.
- Induction of cell cycle arrest via serum deprivation and restimulation.
Main Results:
- IFN treatment decreased Ki-67 expression in GO/G1-arrested Daudi cells, correlating with growth arrest.
- No significant change in Ki-67 expression was observed in IFN-resistant Namalwa cells or S-phase-arrested 251 MG cells.
- Serum deprivation abolished Ki-67 expression in 251 MG cells, with expression resuming upon restimulation and S-phase entry.
Conclusions:
- Ki-67 antigen downregulation is cell-cycle and IFN-sensitivity dependent.
- Ki-67 is not a universally reliable marker for monitoring clinical responses to interferon therapy across all cancer types.
Abstract:
The effects of interferon (IFN) on the expression of the nuclear antigen Ki-67 were studied in the two IFN-sensitive tumour cell lines Daudi and 251 MG, known to be arrested in the cell cycle in separate stages. The GO/G1-arrested Burkitt's lymphoma cell line Daudi displayed an increasing fraction of Ki-67 negative cells with time, concomitant with an increasing proportion of growth arrested cells. A small fraction of Ki-67 positive cells were found mainly arrested in G2/M. In contrast, no effect on Ki-67 expression was seen in IFN-resistant Namalwa cells, nor in the sensitive glioma cell line 251 MG, which is blocked in the S phase of the cell cycle. Agents blocking the cells in other phases of the cycle did not affect Ki-67 expression. However, after serum deprivation, no Ki-67 expression was found in the glioma cell line, while restimulation initiated expression after 12 hours as cells entered the S phase. We conclude that the Ki-67 antigen was not down regulated in all cells inhibited by IFN and thus does not seem to be useful to monitor clinical effects of IFN treatment.
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