Abstract:
:Paclitaxel (taxol) has been used for the treatment of various human tumors and is an exceedingly efficient chemotherapy agent against esophageal cancer. However, the precise molecular mechanisms of paclitaxel effects on human esophageal adenocarcinoma cells are not well understood. MTT assay and cell cycle analysis were performed to examine the mechanism of antiproliferative and cell viability effects of paclitaxel in human esophageal adenocarcinoma cancer cells. Western blotting was also used to examine the cell cycle- and apoptosis-related proteins. Paclitaxel inhibited the proliferation of SKGT4 cells in a dose- and time-dependent manner with G2/M arrest. In addition, paclitaxel induced apoptosis through the activation of caspase-3 followed by PARP degradation. In conclusion, our results suggest that paclitaxel leads to mitotic cell cycle arrest following G2/M arrest and induces apoptosis via a caspase-3 pathway in SKGT4 cells.
journal_name
Int J Oncoljournal_title
International journal of oncologyauthors
Kim SJ,Chung MJ,Kim JS,Kim B,Park WH,Kim SH,Kim SZ,Lee JS,Kim SMdoi
10.3892/ijo.2011.1135subject
Has Abstractpub_date
2011-12-01 00:00:00pages
1587-91issue
6eissn
1019-6439issn
1791-2423journal_volume
39pub_type
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