Cell recycling protects tumor cells from anti-cancer therapy

Mar 06, 2008

Cells have their own recycling system: Discarded cellular components, from individual proteins through to whole cellular organs, are degraded and the building blocks re-used in a different place. The scientific term for this recycling process is autophagy. In severely damaged cells, autophagy can also be a form of programmed cell death. In this case, the cell uses the mechanism for complete self-decomposition.

Cancer cells, too, make use of autophagy – especially after radiation or chemotherapy. However, why autophagy is activated in this context, is not clear. It is possible that the process contributes to the death of the treated tumor cells. But autophagy might also be an attempt by the cells to survive. “Autophagy is also switched on specifically, for example, when the cell does not have enough nutrients at its disposal,” explains Professor Ingrid Herr, head of the Research Group “Molecular OncoSurgery” of the German Cancer Research Center.

Working together with Dr. Anja Apel and scientists of the University of Tübingen, Ingrid Herr has studied the role of autophagy in cancer treatment. To this end, the investigators switched off a number of genes in tumor cells that are essential for autophagy.

Subsequently, they irradiated the cells and then examined how many cells had survived the treatment. They found out that cells that had been almost completely resistant to radiation became more sensitive to radiotherapy due to blocked autophagy. No effect was found on cancer cells that had already responded well to radiotherapy before.

Therefore, the researchers assume that highly aggressive cancer cells use autophagy to resist tumor therapy. The Heidelberg researchers will now investigate whether blocking the recycling system might be useful to support anti-cancer therapies.

Source: Helmholtz Association of German Research Centres

Explore further: Research identifies a way to make cancer cells more responsive to chemotherapy

add to favorites email to friend print save as pdf

Related Stories

How cells know when it's time to eat themselves

Jan 17, 2013

Researchers at the University of California, San Diego School of Medicine have identified a molecular mechanism regulating autophagy, a fundamental stress response used by cells to help ensure their survival ...

Cell biology: Flushing out fats

Dec 19, 2012

The Wip1 protein is important for survival, but mutations that inactivate it carry some surprising features. "A lack of Wip1 results in an excessive immune reaction to infectious organisms, in some cases ...

Scientists discover how two proteins help keep cells healthy

Dec 02, 2012

Scientists at The Scripps Research Institute (TSRI) have determined how two proteins help create organelles, or specialized subunits within a cell, that play a vital role in maintaining cell health. This discovery opens the ...

US computer graphics scientist wins Kyoto Prize

Nov 10, 2012

An American regarded as a father of computer graphics, an Indian literary critic and a Japanese molecular cell biologist have received the Kyoto Prize, Japan's highest private award for global achievement.

Recommended for you

Mayo Clinic genomic analysis lends insight to prostate cancer

8 hours ago

Mayo Clinic researchers have used next generation genomic analysis to determine that some of the more aggressive prostate cancer tumors have similar genetic origins, which may help in predicting cancer progression. The findings ...

User comments : 0

More news stories

Controlling mood through the motions of mitochondria

(Medical Xpress)—Regulating the distribution of power in neurons is done by a system that makes the national electric grid look simple by comparison. Each neuron has several thousand mitochondria confined ...

A quantum simulator for magnetic materials

Physicists understand perfectly well why a fridge magnet sticks to certain metallic surfaces. But there are more exotic forms of magnetism whose properties remain unclear, despite decades of intense research. ...