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Differential expression of the p27Kip1 mRNA in IFN-sensitive and resistant cell lines

A Moro¹, A Calixto, E Suárez

¹División de Farmacéuticos, Centro de Ingeniería Genética y Biotecnología (CIGB), Ciudad de La Habana, Cuba. farma@ingen.cigb.edu.cu

Biochemical and Biophysical Research Communications

|May 20, 1998

Abstract:

IFNs arrest the growth of a small cell lung cancer (SCLC) cell line NCI-H82 in the G1 phase but not the growth of the derived cell line NCI-H82R. Progression through the G1 phase is controlled by positive and negative regulatory genes. Oncoviral genes can override this control. In this study, we compared the effects of human IFN alpha 2b on the mRNA levels of the Cdk inhibitor p27Kip1 in NCI-H82, NCI-H82R and HPV 16 E7-transfected NCI-H82 cell lines. Induction of the 2-5 Oligoadenylate synthetase (2-5 OAS) gene was used as a marker of IFN-dependent signal transduction The expression of p27Kip1 mRNA increased at 48 and 72 hr after IFN alpha 2b addition in sensitive cells. In contrast, p27Kip1 mRNA had only slight variations in both the resistant and E7-transfected cells. Interestingly, the E7-transfected NCI-H82 cells became resistant to the IFN alpha 2b anti-proliferative effect. Our results suggest that p27Kip1 could be a key mediator of the IFN alpha 2b-induced growth arrest and that HPV 16 E7 might affect p27Kip1 inducibility, originating IFN alpha 2b-resistant cells.

Insights

Interferons (IFNs) halt small cell lung cancer (SCLC) cell growth by increasing p27Kip1 mRNA. Human Papillomavirus type 16 E7 (HPV 16 E7) oncoprotein confers resistance to IFNs by inhibiting this effect.

Area of Science:

Oncology
Virology
Molecular Biology

Background:

Interferons (IFNs) exhibit anti-proliferative effects on cancer cells, including small cell lung cancer (SCLC).
Cell cycle progression is tightly regulated by gene networks, which can be disrupted by viral oncoproteins.
Understanding mechanisms of IFN resistance is crucial for developing effective cancer therapies.

Purpose of the Study:

To investigate the role of p27Kip1 mRNA in IFN alpha 2b-induced growth arrest in SCLC cells.
To determine if Human Papillomavirus type 16 E7 (HPV 16 E7) oncoprotein influences IFN sensitivity.
To compare IFN effects on p27Kip1 expression in sensitive and resistant SCLC cell lines.

Main Methods:

Treatment of NCI-H82 (SCLC) and derived NCI-H82R cells with human IFN alpha 2b.
Transfection of NCI-H82 cells with HPV 16 E7 gene.
Quantification of p27Kip1 and 2-5 Oligoadenylate synthetase (2-5 OAS) mRNA levels using quantitative methods.
Assessment of cell proliferation and IFN sensitivity.

Main Results:

IFN alpha 2b treatment significantly increased p27Kip1 mRNA levels in sensitive NCI-H82 cells at 48 and 72 hours.
Resistant NCI-H82R and HPV 16 E7-transfected NCI-H82 cells showed minimal changes in p27Kip1 mRNA expression upon IFN alpha 2b treatment.
HPV 16 E7-transfected cells acquired resistance to the anti-proliferative effects of IFN alpha 2b.

Conclusions:

p27Kip1 is a key mediator of IFN alpha 2b-induced growth arrest in SCLC.
HPV 16 E7 oncoprotein may confer IFN resistance by downregulating p27Kip1 inducibility.
Targeting p27Kip1 or overcoming HPV 16 E7-mediated resistance could restore IFN sensitivity in SCLC.

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