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Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE209883 | GEO | 2023/02/25

REPOSITORIES: GEO

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Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C, short-term effects

Project description:Bladder cancer is common and one of the most costly cancer forms, due to a lack of curative therapies. Recently, clinical safety and efficacy of the alpha1-oleate complex was demonstrated in a placebo-controlled study of non-muscle invasive bladder cancer. This study investigated if long-term therapeutic efficacy is improved by repeated treatment cycles and by combining alpha1-oleate with low-dose chemotherapy. Rapidly growing bladder tumors were treated by intravesical instillation of alpha1-oleate, Epirubicin or Mitomycin C alone or in combination. One treatment cycle arrested tumor growth, with a protective effect lasting at least four weeks in mice receiving 8.5 mM of alpha1-oleate alone or 1.7 mM of alpha-oleate combined with Epirubicin or Mitomycin C. Repeated treatment cycles extended protection, defined by a lack of bladder pathology and a virtual absence of bladder cancer-specific gene expression. Synergy with Epirubicin was detected at the lower alpha1-oleate concentration and alpha1-oleate was shown to enhance the uptake and nuclear translocation of Epirubicin, by tumor cells. Effects at the chromatin level affecting cell proliferation were further suggested by reduced BrdU incorporation. In addition, alpha1-oleate triggered DNA fragmentation, defined by the TUNEL assay. The results suggest that bladder cancer development may be prevented long-term in the murine model, by alpha1-oleate alone or in combination with low-dose Epirubicin. In addition, the combination of alpha1-oleate and Epirubicin reduced the size of established tumors. Exploring these potent preventive and therapeutic effects will be of immediate interest in patients with bladder cancer.

2023-02-25 | GSE209882 | GEO

Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C, long-term effects

2023-02-25 | GSE209881 | GEO

Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate.

Project description:Potent chemotherapeutic agents are required to counteract the aggressive behavior of cancer cells and patients often experience severe side effects, due to tissue toxicity. This study addresses if a better balance between efficacy and toxicity can be attained using the tumoricidal complex alpha1-oleate, formed by a synthetic, alpha-helical peptide comprising the N-terminal 39 amino acids of alpha-lactalbumin and the fatty acid oleic acid. Bladder cancer was established, by intra-vesical instillation of MB49 cells on day 0 and the treatment group received five instillations of alpha1-oleate (1.7-17mM) on days 3-11. A dose-dependent reduction in tumor size, bladder size and bladder weight was recorded in the alpha1-oleate treated group, compared to sham-treated mice. Tumor markers Ki-67, Cyclin D1 and VEGF were inhibited in a dose-dependent manner, as was the expression of cancer-related genes. Remarkably, toxicity for healthy tissue was not detected in alpha1-oleate-treated, tumor bearing mice or in healthy mice or rabbits, challenged with increasing doses of the active complex. The results define a dose-dependent therapeutic effect of alpha1-oleate in a murine bladder cancer model.

2020-04-09 | GSE148308 | GEO

Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C

Project description:Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C

| PRJNA862869 | ENA

Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C, short-term effects

Project description:Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C, short-term effects

| PRJNA862873 | ENA

Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C, long-term effects

Project description:Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate alone or in combination Epirubicin or Mitomycin C, long-term effects

| PRJNA862874 | ENA

Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate.

Project description:Expression data from mice bladder with MB49-induced cancer treated with alpha1-oleate.

| PRJNA623875 | ENA

Expression data from mice bladder with MB49-induced cancer treated with Lon protease

Project description:MYC has been named the quintessential oncogene and is deregulated in the majority of human cancers. Still, finding c-MYC inhibitors for therapeutic use has been problematic and MYC itself has long been viewed as “undruggable”. Here we present a novel strategy for achieving c-MYC inhibition, involving specific bacterial effector molecules. We made the surprising observation that uropathogenic E. coli activate c-MYC degradation and attenuate MYC expression in host cells and tissues. We further identified effector molecules responsible for this effect. The bacterial Lon protease is shown to rapidly degrade c-MYC and therapeutic efficacy is demonstrated in bladder and colon cancer models. Long-term protection, defined by delayed tumor progression, increased survival and low toxicity further supports the therapeutic potential of Lon. These results suggest that bacteria have evolved strategies to control c-MYC tissue levels in the host, which can be exploited to target c-MYC therapeutically in different cancers.

2021-02-10 | GSE162251 | GEO

Effects of siRNA Livin on EJ human bladder cancer cells treated with mitomycin-C.

Project description:The aim of this study was to observe the inhibitory and therapeutic effects of small interfering RNA (siRNA) targeting Livin in EJ human bladder cancer cells. Specific siRNA targeting Livin was synthesized and transfected into EJ human bladder cancer cells treated or not treated with mitomycin-C (MMC). Livin mRNA and protein, as well as proliferation and apoptosis of EJ cells was examined with reverse transcription-polymerase chain reaction, western blotting, Cell Counting Kit-8 assay and flow cytometry, respectively. The results indicated that the expression of Livin mRNA and protein in EJ cells was significantly decreased by siRNA Livin. The proliferation of EJ cells was significantly inhibited by treatment with MMC and transfection of siRNA Livin. The inhibition of cell proliferation by treatment with MMC was further enhanced by transfection of siRNA Livin. The apoptotic rate of cells transfected with siRNA Livin and treated with MMC was significantly higher than those cells receiving a single transfection of siRNA Livin and single treatment of MMC. In conclusion, the present study demonstrates that transfection of siRNA Livin induces growth suppression and apoptosis in EJ human bladder cancer cells, and increases the chemotherapeutic sensitivity of cells to MMC.

| S-EPMC4580073 | biostudies-literature

Sex differences in the MB49 syngeneic, murine model of bladder cancer.

Project description:OBJECTIVE:The MB49 syngeneic, murine model of bladder cancer has been widely used for more than 35 years. In humans, bladder cancer is one third as prevalent in women as in men, with a trend toward lower prevalence in parous compared to nulliparous women. Our objective was to determine if the MB49 bladder cancer model reproduces the sex differences observed in humans, and to determine its sensitivity to testosterone and the pregnancy hormone, human chorionic gonadotropin (hCG). METHODS:Male and female C57BL/6 mice were implanted with MB49 murine bladder cancer cells, and observed for tumor growth. MB49 dose responses to hCG and dihydrotestosterone were determined in vitro. RESULTS:MB49 tumor growth was significantly greater in male mice than female mice. Pregnancy did not affect MB49 tumor growth in female mice. MB49 cells did not proliferate in response to hCG in vitro and the functional receptor for gonadotropins was absent. Dihydrotestosterone strongly stimulated growth of MB49 cells in vitro. CONCLUSIONS:The MB49 murine model of bladder cancer reproduced some aspects of the sex differences observed in humans. Our results suggest that testosterone may stimulate MB49 cell proliferation, which may explain the more rapid MB49 tumor growth observed in male mice.

| S-EPMC4795170 | biostudies-literature

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