Abstract
The effects of liposome-encapsulated annamycin (L-Ann) were investigated in two human breast cancer cell lines, MCF7 and MDA-MB-435. For comparative purposes, doxorubicin (Dx) was used throughout the study. A 4-hour treatment with L-Ann was significantly more active in MDA-MB-435 than in MCF7 cells (IC50 values of 0.03 and 0.08 μg/ml, respectively), whereas Dx was equally active in the two cell lines (IC50 0.12 μg/ml). L-Ann induced an accumulation of cells in G2M phases which was dose-dependent in MDA-MB-435 but not in MCF7 cells. Dx also caused a dose-dependent increase of G2M cell fraction in MDA-MB-435 cells, whereas a G2M cell accumulation was observed only after treatment with the highest Dx concentration in MCF7 cells. G2M phase cell accumulations induced in MCF7 cells by L-Ann or Dx were accompanied by a decrease in cdc2 kinase activity and in cyclin B1 and cdc2 expression. Conversely, in MDA-MB-435 cells exposed to L-Ann or Dx, cdc2 kinase activity, cyclin B1 and cdc2 expression increased in parallel to the increase in the number of cells accumulated in the G2M phase. L-Ann and Dx induced apoptosis in MDA-MB-435 but not in MCF7 cells. In MDA-MB-435 cells exposed to L-Ann or Dx, no change was observed in the expression of bax, but there was a p53-independent increase in p21waf1 expression. In MCF7 cells, treatment with L-Ann or Dx induced an increase in p53 expression with a consequent transactivation of p21waf1 and bax. Our results indicate that L-Ann is more cytotoxic than Dx in breast cancer cells and is able to induce apoptosis through p53-independent mechanisms.
| Original language | English |
|---|---|
| Pages (from-to) | 9-22 |
| Number of pages | 14 |
| Journal | Journal of Cellular Biochemistry |
| Volume | 81 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2001 |
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Keywords
- Anthracyclines
- cdc2 kinase
- Cell proliferation
- Flow cytometry
- p53
ASJC Scopus subject areas
- Biochemistry
- Cell Biology
Cite this
Effects of liposome-entrapped annamycin in human breast cancer cells : Interference with cell cycle progression and induction of apoptosis. / Orlandi, Linda; Bertoli, Gloria; Abolafio, Gabriella; Daidone, Maria Grazia; Zaffaroni, Nadia.
In: Journal of Cellular Biochemistry, Vol. 81, No. 1, 2001, p. 9-22.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of liposome-entrapped annamycin in human breast cancer cells
T2 - Interference with cell cycle progression and induction of apoptosis
AU - Orlandi, Linda
AU - Bertoli, Gloria
AU - Abolafio, Gabriella
AU - Daidone, Maria Grazia
AU - Zaffaroni, Nadia
PY - 2001
Y1 - 2001
N2 - The effects of liposome-encapsulated annamycin (L-Ann) were investigated in two human breast cancer cell lines, MCF7 and MDA-MB-435. For comparative purposes, doxorubicin (Dx) was used throughout the study. A 4-hour treatment with L-Ann was significantly more active in MDA-MB-435 than in MCF7 cells (IC50 values of 0.03 and 0.08 μg/ml, respectively), whereas Dx was equally active in the two cell lines (IC50 0.12 μg/ml). L-Ann induced an accumulation of cells in G2M phases which was dose-dependent in MDA-MB-435 but not in MCF7 cells. Dx also caused a dose-dependent increase of G2M cell fraction in MDA-MB-435 cells, whereas a G2M cell accumulation was observed only after treatment with the highest Dx concentration in MCF7 cells. G2M phase cell accumulations induced in MCF7 cells by L-Ann or Dx were accompanied by a decrease in cdc2 kinase activity and in cyclin B1 and cdc2 expression. Conversely, in MDA-MB-435 cells exposed to L-Ann or Dx, cdc2 kinase activity, cyclin B1 and cdc2 expression increased in parallel to the increase in the number of cells accumulated in the G2M phase. L-Ann and Dx induced apoptosis in MDA-MB-435 but not in MCF7 cells. In MDA-MB-435 cells exposed to L-Ann or Dx, no change was observed in the expression of bax, but there was a p53-independent increase in p21waf1 expression. In MCF7 cells, treatment with L-Ann or Dx induced an increase in p53 expression with a consequent transactivation of p21waf1 and bax. Our results indicate that L-Ann is more cytotoxic than Dx in breast cancer cells and is able to induce apoptosis through p53-independent mechanisms.
AB - The effects of liposome-encapsulated annamycin (L-Ann) were investigated in two human breast cancer cell lines, MCF7 and MDA-MB-435. For comparative purposes, doxorubicin (Dx) was used throughout the study. A 4-hour treatment with L-Ann was significantly more active in MDA-MB-435 than in MCF7 cells (IC50 values of 0.03 and 0.08 μg/ml, respectively), whereas Dx was equally active in the two cell lines (IC50 0.12 μg/ml). L-Ann induced an accumulation of cells in G2M phases which was dose-dependent in MDA-MB-435 but not in MCF7 cells. Dx also caused a dose-dependent increase of G2M cell fraction in MDA-MB-435 cells, whereas a G2M cell accumulation was observed only after treatment with the highest Dx concentration in MCF7 cells. G2M phase cell accumulations induced in MCF7 cells by L-Ann or Dx were accompanied by a decrease in cdc2 kinase activity and in cyclin B1 and cdc2 expression. Conversely, in MDA-MB-435 cells exposed to L-Ann or Dx, cdc2 kinase activity, cyclin B1 and cdc2 expression increased in parallel to the increase in the number of cells accumulated in the G2M phase. L-Ann and Dx induced apoptosis in MDA-MB-435 but not in MCF7 cells. In MDA-MB-435 cells exposed to L-Ann or Dx, no change was observed in the expression of bax, but there was a p53-independent increase in p21waf1 expression. In MCF7 cells, treatment with L-Ann or Dx induced an increase in p53 expression with a consequent transactivation of p21waf1 and bax. Our results indicate that L-Ann is more cytotoxic than Dx in breast cancer cells and is able to induce apoptosis through p53-independent mechanisms.
KW - Anthracyclines
KW - cdc2 kinase
KW - Cell proliferation
KW - Flow cytometry
KW - p53
UR - http://www.scopus.com/inward/record.url?scp=0035089655&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035089655&partnerID=8YFLogxK
U2 - 10.1002/1097-4644(20010401)81:1<9::AID-JCB1020>3.0.CO;2-C
DO - 10.1002/1097-4644(20010401)81:1<9::AID-JCB1020>3.0.CO;2-C
M3 - Article
VL - 81
SP - 9
EP - 22
JO - Journal of Cellular Biochemistry
JF - Journal of Cellular Biochemistry
SN - 0730-2312
IS - 1
ER -