New research linking cancer-inhibiting proteins to cell antennae

December 14, 2017

CANCER RESEARCH Danish researchers have just presented a previously unknown mechanism that inhibits the ability of cells to develop into cancer cells. Their findings have important implications for the understanding of how cancer starts, and how to improve the treatment of illness in the future. The discovery is published today in the internationally recognized Journal of Cell Biology.

Under the leadership of Professor Søren Tvorup Christensen and Associate Professor Lotte Bang Pedersen, researchers at the University of Copenhagen's Department of Biology have taken an important step forward in understanding the very complex mechanisms by which the cells in our body are able to maintain their normal function, and how defects in these mechanisms could trigger cancer cell formation.

The researchers began by referencing a previous discovery of their own: certain types of signaling molecules are detected by specific receptors (PDGFRα) in what are known as primary cilia. These cilia are present as single units on nearly all cell types in the human body and they function as cellular antennae that detect and transmit extracellular cues to control embryonic development and maintain tissue and organ function in adults. The research group has now demonstrated that the very same antennae also play a crucial role in the balancing of the output of PDGFRα signaling so that the signaling doesn't get out of control. Unconstrained, excessive signaling from these receptors increases the risk - of brain tumor and gastrointestinal cancer development.

"Our results demonstrate that, under normal conditions, primary cilia serve to inhibit processes that can lead to cancer. We have shown that specific cancer-inhibiting proteins of the Cbl-family mediate the targeting of PDGFRα to the cilia, and once located in these antennae, the Cbl proteins prevent excessive receptor activation. Further, we have demonstrated that stabilization and functionality of the Cbl proteins are regulated by an entirely new mechanism, which also is associated with the cilia. Should this mechanism be disturbed, the Cbl proteins will undergo self-destruction, which in turn will lead to mislocalization of the receptors to the general cell surface from where the receptors are wildly over-activated", according to Professor Christensen.

The result is dramatic because cell antennae will now play an entirely new role in both our understanding of tumor progression and in the development of improved diagnostic and treatment methods for patients affected by certain types of cancer. According to the research group, it is likely that other illnesses are also linked to Cbl-protein protection errors.

- "Defects in Cbl proteins are also associated with leukemia and autoimmune diseases. Therefore, our hope is that this discovery will contribute to a better understanding of the mechanisms that lead to these other very complicated illnesses," concludes Søren Tvorup Christensen.

Faculty of Science - University of Copenhagen

Related Cancer Articles from Brightsurf:

New blood cancer treatment works by selectively interfering with cancer cell signalling
University of Alberta scientists have identified the mechanism of action behind a new type of precision cancer drug for blood cancers that is set for human trials, according to research published in Nature Communications.

UCI researchers uncover cancer cell vulnerabilities; may lead to better cancer therapies
A new University of California, Irvine-led study reveals a protein responsible for genetic changes resulting in a variety of cancers, may also be the key to more effective, targeted cancer therapy.

Breast cancer treatment costs highest among young women with metastic cancer
In a fight for their lives, young women, age 18-44, spend double the amount of older women to survive metastatic breast cancer, according to a large statewide study by the University of North Carolina at Chapel Hill.

Cancer mortality continues steady decline, driven by progress against lung cancer
The cancer death rate declined by 29% from 1991 to 2017, including a 2.2% drop from 2016 to 2017, the largest single-year drop in cancer mortality ever reported.

Stress in cervical cancer patients associated with higher risk of cancer-specific mortality
Psychological stress was associated with a higher risk of cancer-specific mortality in women diagnosed with cervical cancer.

Cancer-sniffing dogs 97% accurate in identifying lung cancer, according to study in JAOA
The next step will be to further fractionate the samples based on chemical and physical properties, presenting them back to the dogs until the specific biomarkers for each cancer are identified.

Moffitt Cancer Center researchers identify one way T cell function may fail in cancer
Moffitt Cancer Center researchers have discovered a mechanism by which one type of immune cell, CD8+ T cells, can become dysfunctional, impeding its ability to seek and kill cancer cells.

More cancer survivors, fewer cancer specialists point to challenge in meeting care needs
An aging population, a growing number of cancer survivors, and a projected shortage of cancer care providers will result in a challenge in delivering the care for cancer survivors in the United States if systemic changes are not made.

New cancer vaccine platform a potential tool for efficacious targeted cancer therapy
Researchers at the University of Helsinki have discovered a solution in the form of a cancer vaccine platform for improving the efficacy of oncolytic viruses used in cancer treatment.

American Cancer Society outlines blueprint for cancer control in the 21st century
The American Cancer Society is outlining its vision for cancer control in the decades ahead in a series of articles that forms the basis of a national cancer control plan.

Read More: Cancer News and Cancer Current Events is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to