Abstract
Inostamycin, which was recently isolated from Streptomyces sp. MH816-AF15 as an inhibitor of cytidine 5′-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, caused a G1-phase accumulation in the cell cycle of small cell lung carcinomas. To investigate whether the cytostatic effect of inostamycin is restricted to lung carcinoma cell lines or applicable to other type of cells, we tested five oral squamous cell carcinoma (SCC) cell lines. Cell growth was suppressed in 62.5-125 ng/ml inostamycin in the culture medium in all oral cancer cell lines tested, with non-viable cells being < 1%, indicating inostamycin is cytostatic on SCC cell lines. Decrease in cyclin D1 mRNA and protein expression due to the inostamycin treatment was accompanied by suppression of phosphorylated retinoblastoma susceptibility gene product (pRB-P) levels. Moreover, flow cytometric analysis showed that inostamycin induced an increase in G1/G0 cells (1.2-3.2 fold) over 24 h. These results suggest that inostamycin is a useful agent for tumour dormant cytostatic therapy for oral SCC.
| Original language | English |
|---|---|
| Pages (from-to) | 613-620 |
| Number of pages | 8 |
| Journal | Cell Biology International |
| Volume | 25 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - 2001 |
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Keywords
- Cyclin D1
- Cytostatic effect
- Inostamycin
- Oral cancer
- Retinoblastoma
ASJC Scopus subject areas
- Cell Biology
Cite this
Cytostatic effect of inostamycin, an inhibitor of cytidine 5′-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG) : Inositol transferase, on oral squamous cell carcinoma cell lines. / Baba, Yuh; Tsukuda, Mamoru; Mochimatsu, Izumi; Furukawa, Shigeru; Kagata, Hiroko; Nagashima, Yoji; Koshika, Shinri; Imoto, Masaya; Kato, Yasumasa.
In: Cell Biology International, Vol. 25, No. 7, 2001, p. 613-620.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cytostatic effect of inostamycin, an inhibitor of cytidine 5′-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG)
T2 - Inositol transferase, on oral squamous cell carcinoma cell lines
AU - Baba, Yuh
AU - Tsukuda, Mamoru
AU - Mochimatsu, Izumi
AU - Furukawa, Shigeru
AU - Kagata, Hiroko
AU - Nagashima, Yoji
AU - Koshika, Shinri
AU - Imoto, Masaya
AU - Kato, Yasumasa
PY - 2001
Y1 - 2001
N2 - Inostamycin, which was recently isolated from Streptomyces sp. MH816-AF15 as an inhibitor of cytidine 5′-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, caused a G1-phase accumulation in the cell cycle of small cell lung carcinomas. To investigate whether the cytostatic effect of inostamycin is restricted to lung carcinoma cell lines or applicable to other type of cells, we tested five oral squamous cell carcinoma (SCC) cell lines. Cell growth was suppressed in 62.5-125 ng/ml inostamycin in the culture medium in all oral cancer cell lines tested, with non-viable cells being < 1%, indicating inostamycin is cytostatic on SCC cell lines. Decrease in cyclin D1 mRNA and protein expression due to the inostamycin treatment was accompanied by suppression of phosphorylated retinoblastoma susceptibility gene product (pRB-P) levels. Moreover, flow cytometric analysis showed that inostamycin induced an increase in G1/G0 cells (1.2-3.2 fold) over 24 h. These results suggest that inostamycin is a useful agent for tumour dormant cytostatic therapy for oral SCC.
AB - Inostamycin, which was recently isolated from Streptomyces sp. MH816-AF15 as an inhibitor of cytidine 5′-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, caused a G1-phase accumulation in the cell cycle of small cell lung carcinomas. To investigate whether the cytostatic effect of inostamycin is restricted to lung carcinoma cell lines or applicable to other type of cells, we tested five oral squamous cell carcinoma (SCC) cell lines. Cell growth was suppressed in 62.5-125 ng/ml inostamycin in the culture medium in all oral cancer cell lines tested, with non-viable cells being < 1%, indicating inostamycin is cytostatic on SCC cell lines. Decrease in cyclin D1 mRNA and protein expression due to the inostamycin treatment was accompanied by suppression of phosphorylated retinoblastoma susceptibility gene product (pRB-P) levels. Moreover, flow cytometric analysis showed that inostamycin induced an increase in G1/G0 cells (1.2-3.2 fold) over 24 h. These results suggest that inostamycin is a useful agent for tumour dormant cytostatic therapy for oral SCC.
KW - Cyclin D1
KW - Cytostatic effect
KW - Inostamycin
KW - Oral cancer
KW - Retinoblastoma
UR - http://www.scopus.com/inward/record.url?scp=0034923063&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034923063&partnerID=8YFLogxK
U2 - 10.1006/cbir.2000.0706
DO - 10.1006/cbir.2000.0706
M3 - Article
C2 - 11448100
AN - SCOPUS:0034923063
VL - 25
SP - 613
EP - 620
JO - Cell Biology International
JF - Cell Biology International
SN - 1065-6995
IS - 7
ER -