Location
University of Nevada Las Vegas, Student Union Ball Room
Start Date
6-8-2009 9:30 AM
End Date
6-8-2009 12:00 PM
Description
The concept of “tumor stem cells” has garnered much attention in the last few years. Tumor stem cells are believed to exist among a heterogeneous group of cells that constitute a tumor. These tumor stem cells often express genes that are important for stem cell function, cell division, and maintenance of pluripotent state in stem cells. Stem cell or stem cell maintenance genes such as SALL 4 and Bmi-1 are often seen in these cancer cells and contribute to self-renewing divisions and cancer cell survival. In particular, high expression of Bmi-1 (B lymphoma mouse Moloney leukemia virus insertion region), a member of the polycomb family of transcription factors, is often associated with poor prognosis in cancers.
Our laboratory has shown the existence of an alternatively spliced Bmi-1 RNA and protein in multiple myeloma cells. The purpose of this research project is to understand the effect of an alternate splice form of Bmi-1 protein on cell cycle and apoptosis in multiple myeloma cells. To understand the effect of this alternate Bmi-1 protein, I first compared the growth rate of different myeloma cell lines and correlated that with the expression of the wild-type Bmi-1 and the alternatively spliced Bmi-1 form. I performed time course experiments and counted the cell numbers in each cell line at various time points. My results show that the myeloma cell lines, which highly express the alternate form of Bmi-1, grew faster than the myeloma cell lines, which mostly express the wild-type form of Bmi-1. Currently I am performing RT-PCR and western blot analysis to confirm the existence of the alternatively spliced Bmi-1 protein. I plan to isolate and sequence the alternatively spliced form of Bmi-1. I also plan to determine the effect of knocking-down Bmi-1 expression on cell cycle and apoptosis by incorporating inducible shRNA viral constructs targeted against Bmi-1 RNA in myeloma cells.
Keywords
Bmi-1 RNA; Cancer research; Cell growth; Tumor stem cells
Disciplines
Cancer Biology | Oncology
Language
English
Expression of an alternate splice form of Bmi-1 in multiple myeloma
University of Nevada Las Vegas, Student Union Ball Room
The concept of “tumor stem cells” has garnered much attention in the last few years. Tumor stem cells are believed to exist among a heterogeneous group of cells that constitute a tumor. These tumor stem cells often express genes that are important for stem cell function, cell division, and maintenance of pluripotent state in stem cells. Stem cell or stem cell maintenance genes such as SALL 4 and Bmi-1 are often seen in these cancer cells and contribute to self-renewing divisions and cancer cell survival. In particular, high expression of Bmi-1 (B lymphoma mouse Moloney leukemia virus insertion region), a member of the polycomb family of transcription factors, is often associated with poor prognosis in cancers.
Our laboratory has shown the existence of an alternatively spliced Bmi-1 RNA and protein in multiple myeloma cells. The purpose of this research project is to understand the effect of an alternate splice form of Bmi-1 protein on cell cycle and apoptosis in multiple myeloma cells. To understand the effect of this alternate Bmi-1 protein, I first compared the growth rate of different myeloma cell lines and correlated that with the expression of the wild-type Bmi-1 and the alternatively spliced Bmi-1 form. I performed time course experiments and counted the cell numbers in each cell line at various time points. My results show that the myeloma cell lines, which highly express the alternate form of Bmi-1, grew faster than the myeloma cell lines, which mostly express the wild-type form of Bmi-1. Currently I am performing RT-PCR and western blot analysis to confirm the existence of the alternatively spliced Bmi-1 protein. I plan to isolate and sequence the alternatively spliced form of Bmi-1. I also plan to determine the effect of knocking-down Bmi-1 expression on cell cycle and apoptosis by incorporating inducible shRNA viral constructs targeted against Bmi-1 RNA in myeloma cells.
Comments
Abstract & poster