Expression of MICA, MICB and NKG2D in human leukemic myelomonocytic and cervical cancer cells
Por:
Weiss-Steider, B, Soto-Cruz, I, Martinez-Campos, CA, Mendoza-Rincon, JF
Publicada:
10 abr 2011
Resumen:
Background: Cancer cells are known to secrete the stress molecules MICA and MICB that activate cytotoxicity by lymphocytes and NK cells through their NKG2D receptor as a mechanism of immunological defense. This work was undertaken to evaluate if cancer cells can also express this receptor as a possible mechanisms of depletion of MIC molecules and thus interfere with their immune recognition. Methods: Myelomonocytic leukemic (TPH-1 and U-937) and cervical cancer (CALO and INBL) cell lines were evaluated by Western Blot, ELISA, flow cytometry and immunocytochemistry to evaluate their capacity to express and secrete MICA and MICB and to be induced to proliferate by these molecules as well as to express their receptor NKG2D. Statistical analysis was performed by two-way ANOVA for time course analysis and Student's t-test for comparison between groups. Values were considered significantly different if p < 0.05. Results: THP-1 and U-937 produce and secrete the stress MICA and MICB as shown b
Filiaciones:
Weiss-Steider, B:
Univ Nacl Autonoma Mexico, Unidad Diferenciac Celular & Canc, FES Zaragoza, Oncol Mol Lab, Mexico City 09230, DF, Mexico
Soto-Cruz, I:
Univ Nacl Autonoma Mexico, Unidad Diferenciac Celular & Canc, FES Zaragoza, Oncol Mol Lab, Mexico City 09230, DF, Mexico
Martinez-Campos, CA:
Univ Nacl Autonoma Mexico, Unidad Diferenciac Celular & Canc, FES Zaragoza, Oncol Mol Lab, Mexico City 09230, DF, Mexico
Mendoza-Rincon, JF:
Univ Nacl Autonoma Mexico, Unidad Diferenciac Celular & Canc, FES Zaragoza, Oncol Mol Lab, Mexico City 09230, DF, Mexico
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