Bmi-1 in the regulation of prostate cancer development


There are a lot of media reports today about a protein called Bmi-1 and its impact on the regulation and development of prostate cancer.

The media furore is based on a paper by Lukacs et al. in the journal Cell Stem Cell and a media release issued by the University of California, Los Angeles. However, the idea that Bmi-1 is a unique “missing link” that causes prostate cancer cells to grow and metastasize (being promulgated by some media) is certainly an over-reaction.

The studies carried out by Lukacs and her colleagues certainly add to our understanding of the effects of Bmi-1 in prostate cancer. But they are laboratory and animal studies, not human studies, and the findings need to be interpreted with the usual caution.

Expression of Bmi-1 is often up-regulated in prostate cancer. In other words, cells make more of the protein that they do in normal prostate cells. In addition, expression of Bmi-1 is already believed to be associated with the presence of prostate cancers of higher Gleason grade, and this means it is associated with cancers that have a relatively poor prognosis.

What Lukacs and her colleagues have really been able to show in their recent study is three things:

  • Expression of Bmi-1 expression seems to be essential for self-renewal activity and maintenance of prostate stem cells with highly proliferative abilities.
  • Loss of Bmi-1 expression blocks the self-renewal activity, protecting prostate cells from abnormal changes in growth that can lead to cancer.
  • Inhibition of the expression of Bmi-1 slowed the growth of an aggressive form of prostate cancer in animal models.

Owen Witte, the senior author of the study is quoted in the UCLA media release as follows: “We conclude … that Bmi-1 is a crucial regulator of self-renewal in adult prostate cells and plays important roles in prostate cancer initiation and progression. It was encouraging to see that inhibiting this protein slows the growth of even a very aggressive prostate cancer, because that could give us new ways to attack this disease.”

The bottom line is that by being able to manipulate the expression of Bmi-1, we may be able to develop new drugs that can help to prevent or control growth of prostate cancer cells, but it will take a great deal more work to discover whether such a process is even possible, and then to discover specific therapies based on this idea that are effective and safe in humans. Don’t hold your breathe.

2 Responses

  1. Thanks as always for bringing these developments to our awareness.

    This is clearly preliminary, but I find it quite interesting. I just did a PubMed search, and I got 348 hits with the following search string: “Bmi-1 NOT (body mass index OR weight OR body OR metabolic).” I was especially interested in whether any drugs were being used to affect Bmi-1 and whether it was a hot area in research.

    Though my reading of the first hundred titles (most recent research) did not reveal any drugs, I was impressed that Bmi-1 has been linked to a many other cancers.

    I was also impressed that the bulk of research has been done from 2007 to date and that interest is clearly rising. I tacked on a date element to the search string, such as ” … AND 2009 [dp] “, and found the following. I totaled results and observed that the total was about 380, leading me to think that 32 hits were double counted, probably as printed publication dates and advance epub dates. Here are the hits by year:

    2009 — 64; 2008 — 60; 2007 — 45; 2006 — 29; 2005 — 29; 2004 — 16; 2003 — 13; 2002 — 3; 2001 — 5; 2000 — 6; 1999 — 7; 1998 — 4; 1997 — 3; 1996 — 5; 1995 — 4; 1994 — 4; 1993 — 7; 1992 — 4; 1991 — 7; and none in 1990 and 1989.

    The numerous cancers affected and the increasing vigor of research are encouraging.

  2. Dear Jim:

    You clearly need more to occupy your time! Yes, the potential role of Bmi-1 in several forms of cancers has been well documented. The practical value of this knowledge in translational research has not been well defined as yet.

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