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Elects of taxol and ionizing radiation on cytotoxicity and prostaglandin production in KB, RPMI-2650, SW-13 and L929

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Abstract

Çѱ¹¼¼Æ÷ÁÖÀºÇà¿¡¼­ ºÐ¾ç¹ÞÀº 3Á¾ÀÇ ÀÎü ¾Ï¼¼Æ÷ÁÖ(KB. RPMI-2650, SW-13)¿Í 1Á¾ÀÇ »ý
Áã ¼¶À¯¸ð¼¼Æ÷ÁÖ(L929)¸¦ ¹è¾çÇÏ¿© ´Ù¾çÇÑ ³óµµ(5, 50, 100, 200, 300, 500 nM)ÀÇ taxol·Î ó
¸®ÇÑ ÈÄ 1ÀÏÈÄ¿Í 4 ÀÏÈÄ¿¡ MTTºÐ¼®¹ýÀ¸·Î ¼¼Æ÷»ýÁ¸À²À» ±¸ÇÏ¿© ¼¼Æ÷µ¶¼º º¯È­¸¦ °üÂûÇÏ¿´
À¸¸ç ¶ÇÇÑ 500 nM taxol󸮱º, 10 Gy ¹æ»ç¼±Á¶»ç±º, µÎ °¡ÁöÀÇ º´Çà󸮱º¿¡¼­ °¢¼¼Æ÷ÁÖ
ÀÇ ¼¼Æ÷»ýÁ¸À²°ú prostaglandin Áß PGE2¿Í PGI2ÀÇ ¾çÀ» ÃøÁ¤ÇÏ
¿© ´ÙÀ½°ú °°Àº °á·ÐÀ» ¾ò¾ú´Ù.
1. KB ¼¼Æ÷¿¡¼­´Â taxoló¸® 1Àϱº¿¡ ºñÇØ 4Àϱº¿¡¼­ ¼¼Æ÷µ¶¼ºÀÌ Áõ°¡ÇÏ¿´À¸¸ç ¾ç±º ¸ðµÎ
¿¡¼­ taxol ³óµµ¿Í ¼¼Æ÷µ¶¼º°£¿¡ ³ôÀº »ó°ü°ü°è¸¦ º¸¿´´Ù(1Àϱº R=0.82741, 4Àϱº
R=0.84655).
2. RPMI-2650 ¼¼Æ÷¿¡¼­´Â °í³óµµ taxol󸮱º¿¡¼­¸¸ 1Àϱº¿¡ ºñÇØ 4Àϱº¿¡¼­ ¼¼Æ÷µ¶¼ºÀÌ
Áõ°¡ÇÏ¿´À¸¸ç 4Àϱº¿¡¼­ taxol³óµµ¿Í ¼¼Æ÷µ¶¼º°£¿¡ ¸Å¿ì ³ôÀº »ó°ü°ü°è¸¦ º¸¿´´Ù
(R=0.93917).
3. SW-13 ¼¼Æ÷¿¡¼­´Â Àú³óµµ taxol󸮱ºÀ» Á¦¿ÜÇÏ°í´Â 1Àϱº¿¡ ºñÇØ 4Àϱº¿¡¼­ ¼¼Æ÷µ¶
¼ºÀÌ Áõ°¡ÇÏ¿´À¸¸ç ¾ç±º ¸ðµÎ¿¡¼­ taxol³óµµ¿Í ¼¼Æ÷µ¶¼º°£¿¡ ³ôÀº »ó°ü°ü°è¸¦ º¸ÀÌÁö ¾Ê¾Ò
´Ù (1Àϱº R=0.46362, 4Àϱº R=0.65425).
4. L929 ¼¼Æ÷¿¡¼­´Â Àú³óµµ taxol󸮱º¿¡¼­ ¸¸ 1Àϱº¿¡ ºñÇØ 4Àϱº¿¡¼­ ¼¼Æ÷µ¶¼ºÀÌ Áõ°¡
ÇÏ¿´À¸¸ç taxol³óµµ¿Í ¼¼Æ÷µ¶¼º°£¿¡ »ó°ü°ü°è´Â ¸Å¿ì ³·¾ÒÀ¸¸ç (1Àϱº R=0.34237. 4Àϱº R=
0.23381) L929 1ÀϱºÀ» Á¦¿ÜÇÏ°í´Â 10Gy ¹æ»ç¼±Á¶»ç±º¿¡ ºñÇØ 500nM taxol󸮱º¿¡¼­ ¼¼Æ÷
µ¶¼ºÀÌ ÄÇÀ¸¸ç L929 1Àϱº¿¡¼­¸¸ taxolÀÇ ¹æ»ç¼± Áõ°¨È¿°ú¸¦ °üÂûÇÒ ¼ö ÀÖ¾ú´Ù.
5. ¸ðµç ¾Ï¼¼Æ÷ÁÖ¿¡¼­´Â º´Çàó¸® 4Àϱº¿¡¼­ ¿©·¯ °³ÀÇ ºÐ¿­µÈ ÇÙ°ú ¸¹Àº ºÎÀ¯¼¼Æ÷µéÀÌ
°üÂûµÇ¾úÀ¸³ª L929 ¼¼Æ÷¿¡¼­´Â ´õ ³ôÀº ¼¼Æ÷ Ãæ¹Ðµµ¸¦ º¸¿´À¸¸ç ºÐ¿­µÈ ÇÙÀ̳ª ºÎÀ¯¼¼Æ÷´Â
°üÂûÇÒ ¼ö ¾ø¾ú´Ù.
6. PGE2´Â KB ¼¼Æ÷¿¡¼­ °¡Àå ¸¹ÀÌ °ËÃâµÇ¾úÀ¸¸ç ¸ðµç ¾Ï¼¼Æ÷ÁÖ´Â ½ÇÇ豺
ÀÌ ´ëÁ¶±º¿¡ ºñÇØ Áõ°¡ ÇÏ¿´À¸³ª L929 ¼¼Æ÷¿¡¼­´Â °¨¼ÒÇÏ¿´°í SW-13 ¼¼Æ÷¿¡¼­¸¸ º´Çàó¸®
±ºÀÌ ´Ù¸¥ ±º¿¡ ºñÇØ À¯ÀǼº ÀÖ°Ô Áõ°¡ÇÏ¿´´Ù. PGI2´Â RPMI-2650 ¼¼Æ÷¿¡¼­
°¡Àå ¸¹ÀÌ °ËÃâµÇ¾úÀ¸¸ç SW-13 ¼¼Æ÷¸¦ Á¦¿ÜÇÏ°í´Â ¸ðµÎ Áõ°¡ÇÏ¿´°í RPMI-2650 ¼¼Æ÷¿¡¼­
¸¸ º´Çà󸮱º¿¡¼­ ´Ù¸¥ ±º¿¡ ºñÇØ À¯ÀǼº ÀÖ°Ô Áõ°¡ÇÏ¿´´Ù.
#ÃÊ·Ï#
The author evaluated the effects of taxol, a microtubular inhibitor, as a possible
radiation.
sensitizer and the production of prostaglandins on three human cancer cell lines(KB,
RPMI-2650 and SW-13) and one murine cell line(L929). Each cell line was divided into
four groups(control, taxol only, radiation only and combination of taxol and radiation).
The treatment consisted of a single irradiation of 10 Gy and graded doses(5, 50, 100,
200, 300, 500 nM) of taxol for a 24-h period. The cytotoxicity of taxol alone was
measured at 1 day after(1-day group) and 4 days after(4-day group) the treatment. The
survival ratio of cell was analyzed by MTT (3-(4,5-dimethylthiazol-2-yl) -2,5-dimethyl
tetrazolium bromide) test. Prostaglandins(PGE2 and PGI2) were measured in the culture
medium by a radioimmunoassay.
The results obtained were as follows.
1. There was a significantly increased cytotoxicity of KB cells in 4-day group than
those in 1-day group. There was a high correlation between doses of taxol and cell
viability in both groups(1-day group R=0.82741, 4-day group R=0.84655).
2. There was a significantly increased cytotoxicity of RPMI-2650 cells treated with
high concentration of taxol in 4-day group than those in 1-day group, Also there was a
high correlation between doses of taxol and cell viability in 4-day group (R=0.93917).
3. There was a significantly increased cytotoxicity of SW-13 cells treated with high
concentration of taxol in 4-day group than those in 1-day group. However no high
correlation was observed between doses of taxol and cell viability in both groups(1-day
group R=0.46362, 4-day group R=0.65425).
4. There was a significantly increased cytotoxicity of L929 cells treated with low
concentration of taxol in 4-day group than those in 1-day group. At the same time,
there was a low correlation between doses of taxol and cell viability in both
groups(1-day group R=0.34237, 4-day group R=0.23381).
5. In 1-day group of L929 cells, higher cytotoxicities were observed in the groups
treated with 500 nM taxol than given 10 Gy radiation alone. L929 cells in 1-day group
alone showed a radiosensitizing effect by taxol.
6. In addition to L929 cells, all cancer cells treated with a combination of taxol and
radiation in 4-day group appeared to have some fragmented nuclei and to float on the
medium. In addition, L929 cells appeared to be more confluent.
7. The level of PGE2 production was the highest in the control KB cells.
This appeared to increase in every experimental group of all three cancer cells except
L929 cells. There was a significantly increased production of PGE2 in
SW-13 cells treated with a combination taxol and radiation compared to the other
experimental groups.
8. The level of PGI2 production in the control group of RPMI-2650 cells
was the highest. This appeared to increase in every experimental group of all cells
except in SW-13 cells. This also increased significantly in RPMI-2650 cells treated with
a combination of taxol and radiation compared to the other experimental groups.

irradiation; MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-dimethyltetrazolium bromide); taxal(paclitaxel); prstalandins;

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