Abstract:
:The presence and the involvement of cancer stem-like cells (CSCs) in tumor initiation and progression, and chemo-resistance are documented. Herein, we functionally analyzed melanoma stem-like cells (MSC)/CD133(+) cells on their resistance and response to taxol-induced apoptosis. Besides being taxol resistant, the CD133(+) cells demonstrated a growth advantage over the CD133(-) subpopulation. Taxol induced apoptosis on CD133(-) cells, but not on CD133(+) cells. In the CD133(-) subpopulation, the exposure to taxol induced the activation of apoptosis signal-regulating kinase1 (ASK1)/c-jun-N-terminal kinase (JNK), p38, extracellular signal regulated kinase (ERK) pathways and Bax expression, while in CD133(+) cells taxol was able only to enhance the activity of the ERK pathway. In CD133(+) cells, the direct gene transfer of Bax overcame the acquired resistance to taxol. Taken together, our data provide an insight into the mechanistic cascade of melanoma resistance to taxol and suggest Bax gene transfer as a complementary approach to chemotherapy.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
El-Khattouti A,Selimovic D,Haïkel Y,Megahed M,Gomez CR,Hassan Mdoi
10.1016/j.canlet.2013.09.024subject
Has Abstractpub_date
2014-02-01 00:00:00pages
123-33issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(13)00693-9journal_volume
343pub_type
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