Abstract
Reduction of mitomycin C resistance in human bladder cancer T24 cells by knocking-down ras oncogene
Highlights
Bladder cancer is one of the leading causes of cancer-related death in the world[1]
The intensity of ras and ERK immunoreactivity in T24 cells significantly increased 24 h after treatment with mitomycin C (MMC) doses ≥ 10 μg/mL, compared with that of untreated cells. This suggests enhanced ras protein synthesis countering the anti-proliferative effects of MMC (P < 0.001 for all)
We investigated the synergistic antitumor effects of low doses of MMC and pan-ras siRNA in T24 bladder cancer cells that had previously been reported to be MMCresistant[23]
Summary
Bladder cancer is one of the leading causes of cancer-related death in the world[1]. Despite the increasing number of studies in recent years, the recurrence and progression of bladder cancer remains a challenge. The standard treatment for non-muscle-invasive transitional cell carcinoma of the bladder (TCCB) is transurethral resection and adjuvant intravesical chemotherapy or immunotherapy[2,3]. Clinical effectiveness of mitomycin C (MMC) is often limited by the emergence of drug-resistant tumor cells[4,5]. 43% of the non-muscle-invasive bladder cancer relapses and about 8% progress to muscle-invasive disease[6]
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