Abstract
In human pancreatic carcinoma cells (HPC-4), a hyperthermic treatment at 43 °C for 30 min resulted in the vigorous induction of Hsp72, along with a less pronounced increase in the rate of synthesis of Hsp90, Hsp60 and Hsp 27. Biotinylation of surface-exposed proteins, followed by isolation of biotin-tagged proteins by affinity chromatography, demonstrated that both Hsp72 and Hsp60 are expressed on plasma membrane. Membrane expression of these two Hsps was confirmed by immunoprecipitation of surface biotinylated proteins with anti-Hsp72 and anti-Hsp60 specific antibodies. Cytotoxic assays showed that untreated HPC-4 cells are intrinsically resistant to NK-mediated lysis, while they were efficiently killed by LAK lymphocytes, as well as by exposure to TNFα. Following heat-treatment, cells became much more resistant to LAK-mediated lysis, while their sensitivity to NK-mediated lysis and to TN-Fα cytotoxicity remained unmodified.
| Original language | English |
|---|---|
| Pages (from-to) | 329-334 |
| Number of pages | 6 |
| Journal | Journal of Experimental and Clinical Cancer Research |
| Volume | 19 |
| Issue number | 3 |
| Publication status | Published - 2000 |
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Keywords
- Hsp60
- Hsp72
- Human pancreatic cancer cells
- LAK-mediated cytotoxicity
ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Induction and membrane expression of heat shock proteins in heat-treated HPC-4 cells is correlated with increased resistance to LAK-mediated lysis. / Vendetti, S.; Cicconi, R.; Piselli, P.; Vismara, D.; Cassol, M.; Delpino, A.
In: Journal of Experimental and Clinical Cancer Research, Vol. 19, No. 3, 2000, p. 329-334.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Induction and membrane expression of heat shock proteins in heat-treated HPC-4 cells is correlated with increased resistance to LAK-mediated lysis
AU - Vendetti, S.
AU - Cicconi, R.
AU - Piselli, P.
AU - Vismara, D.
AU - Cassol, M.
AU - Delpino, A.
PY - 2000
Y1 - 2000
N2 - In human pancreatic carcinoma cells (HPC-4), a hyperthermic treatment at 43 °C for 30 min resulted in the vigorous induction of Hsp72, along with a less pronounced increase in the rate of synthesis of Hsp90, Hsp60 and Hsp 27. Biotinylation of surface-exposed proteins, followed by isolation of biotin-tagged proteins by affinity chromatography, demonstrated that both Hsp72 and Hsp60 are expressed on plasma membrane. Membrane expression of these two Hsps was confirmed by immunoprecipitation of surface biotinylated proteins with anti-Hsp72 and anti-Hsp60 specific antibodies. Cytotoxic assays showed that untreated HPC-4 cells are intrinsically resistant to NK-mediated lysis, while they were efficiently killed by LAK lymphocytes, as well as by exposure to TNFα. Following heat-treatment, cells became much more resistant to LAK-mediated lysis, while their sensitivity to NK-mediated lysis and to TN-Fα cytotoxicity remained unmodified.
AB - In human pancreatic carcinoma cells (HPC-4), a hyperthermic treatment at 43 °C for 30 min resulted in the vigorous induction of Hsp72, along with a less pronounced increase in the rate of synthesis of Hsp90, Hsp60 and Hsp 27. Biotinylation of surface-exposed proteins, followed by isolation of biotin-tagged proteins by affinity chromatography, demonstrated that both Hsp72 and Hsp60 are expressed on plasma membrane. Membrane expression of these two Hsps was confirmed by immunoprecipitation of surface biotinylated proteins with anti-Hsp72 and anti-Hsp60 specific antibodies. Cytotoxic assays showed that untreated HPC-4 cells are intrinsically resistant to NK-mediated lysis, while they were efficiently killed by LAK lymphocytes, as well as by exposure to TNFα. Following heat-treatment, cells became much more resistant to LAK-mediated lysis, while their sensitivity to NK-mediated lysis and to TN-Fα cytotoxicity remained unmodified.
KW - Hsp60
KW - Hsp72
KW - Human pancreatic cancer cells
KW - LAK-mediated cytotoxicity
UR - http://www.scopus.com/inward/record.url?scp=0033765035&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033765035&partnerID=8YFLogxK
M3 - Article
VL - 19
SP - 329
EP - 334
JO - Journal of Experimental and Clinical Cancer Research
JF - Journal of Experimental and Clinical Cancer Research
SN - 0392-9078
IS - 3
ER -