EGCG blocks three Polycomb repressor genes

Thanks to a fabulous blog reader, I was able to read the entire text of a recently-published “Carcinogenesis” study on how EGCG, the main polyphenol in green tea, affects not one, not even two, but THREE (!) of the pesky Polycomb repressor genes that play central roles in myeloma. The study examines skin cancer cells, not myeloma ones, but the findings are certainly relevant for us, too. Here is the link to the abstract:

We have already spent a lot of time on EZH2 (see previous posts), which is closely linked to the proliferation (etc.) of myeloma cells, so I won’t bother going over that one again.

But this is the first time we have dealt with Bmi-1 in connection with myeloma. All we need to do is take a look at the title of another study (abstract: “The Polycomb Group Protein Bmi-1 Is Essential for the Growth of Multiple Myeloma Cells.” This part says it all: “…essential for the growth of myeloma cells…” 👿

As for SUZ12, this Polyhooligan* (*this word does not exist, by the way…it just popped into my head as I was writing one of my Polycomb posts) is also super-active in multiple myeloma and, e.g., chronic myeloid leukemia. I became aware of its existence while going through the study that began my Polycomb quest: This study mentions that SUZ12 is significantly correlated with the establishment and progression of MM. Eeek! 

So let’s have a look at the “Carcinogenesis” study. Today I don’t feel like quoting and commenting on huge portions of a study, so I will be amazingly brief…for a change. 🙂

In the abstract, you can read about EGCG’s anticancer activities…I wanted to highlight only that it inhibits some of myeloma’s best buddies—cyclin D1 and so on. Yes, you are right: the abstract is not easy to read (…you should see the full study!…Mamma mia!). In a nutshell, though, it tells us that EGCG reduces the survival of skin cancer cells by decreasing the mad activity of two Polyhooligans, Bmi-1 and EZH2. The third Polyhooligan, SUZ12, is discussed only in the full study (a bit of technical information: SUZ12 belongs to the PCR2 group).

Full study, now. It points out that EGCG has not (yet!) been studied in connection with the hyperactive Polycomb repressor genes. Other studies have shown that EGCG blocks the growth and indeed increases apoptosis in skin cancer cells (apoptosis is the process of programmed cell death). This study shows that expression of prosurvival PcG proteins is increased in skin cancer cells as compared with normal and that EGCG treatment of the cancer cells suppresses PcG protein expression and histone methylation leading to reduced cell survival. Basically, this means that skin cancer cells contain a whole bunch of these hyperactive Polyhooligans, which help them survive…but most of them begin dying as soon as EGCG enters the picture. Not bad, eh! 

Skipping a lot of details (a promise is a promise…!) and getting to the Conclusion: by reducing the hyperactivity of the three above-mentioned Polyhooligans, EGCG is able to have a huge impact on the survival of skin cancer cells. Gollywobbly!

Well, one thing is for sure: I am definitely a coffee-in-the-morning drinker, not a tea-drinker (except when we are in the UK)…but, after reading this study, I am seriously thinking of having a mid-afternoon cup of green tea every day…in fact, it is mid-afternoon right now, sooo…off I go, ciao! 😉


  1. Google translation of a German text of the University of Freiburg:

    Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol in green tea has antitumor, anti-inflammatory and anti-oxidative effects (Navarro-Peran, Cabezas-Herrera et al. 2005; Shammas, Neri et al. 2006) . In accordance with previous work, we were also able to detect a concentration-cytotoxicity and inhibition of proliferation with EGCG on all three myeloma cell lines. As EGCG showed concentrations of 250 mu.M a statistically
    significant increase in PI-positive cells and a significant decrease in vital cells. Our other work and support the further study of multiple myeloma and EGCG
    other tumors. R. Burger et al. was shown) with EGCG concentrations from 6.25 to 100 mu.M a concentration-and time-dependent inhibition of proliferation of various myeloma cell lines, six (including the IL-6-dependent INA-6 cell line. These were the IC50 values of 12.5 to 50 mu.M. Similar concentrations of EGCG could inhibit the IL-6-mediated growth of INA-6 cells and IL-6 could not protect against EGCG-induced cytotoxicity. In INA-6 cells EGCG led to concentration-dependent inhibition
    of IL-6-STAT3 signaling pathway mediated (Burger, et al Czekalla. 2007). Navarro-Peran, E. et al. examined other possible anticarcinogenic mechanisms of action of EGCG (at concentrations
    0-100 mu.M) in vitro and were able to show low concentrations of EGCG (0.1 to 1.0 mu.M) inhibition of dihydrofolate reductase (DHFR) activity, which the thymine and purine synthesis, the tetrahydrofolate (THF) need , is prevented. Thus, they could by DHFR inhibition the concentration dependent cytotoxic effect of EGCG (IC50: 20?M) explain to the lymphoma cell line L1210 (Navarro-Peran, Cabezas-Herrera et al. 2005). Another
    postulated mechanism for the antitumor effect of EGCG on the production of cytotoxic reactive oxygen species (ROS: free radicals) (Navarro-Peran, Cabezas-Herrera et al. 2005).

  2. I don’t know about gum Sandy but you can get green tea tablets. The ones I have are supposed to contain 40% catechins.

  3. Hi, Margaret
    I’ve been following you for awhile but just now signed up to read your entire blog roll! In the meantime, I wondered if you’ve mentioned/researched low dose naltroxene? I have MGUS which is sitting on the edge of MGUS and AMM and am wondering about taking naltroxene.

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