New study shows promise for preventing therapy resistance in tumor cells

by Allison Perry

A new study led by University of Kentucky researchers suggests that activating the tumor suppressor p53 in normal cells causes them to secrete Par-4, another potent tumor suppressor protein that induces cell death in cancer cells. This finding may help researchers decipher how to inhibit the growth of tumors that have become resistant to other treatments.

Loss of the often contributes to therapy resistance in tumors. In the study, published in Cell Reports, the University of Kentucky's Vivek Rangnekar and his colleagues activated wild type p53 in to trigger cell death in the p53-deficient cancer cells. Because p53 is intact and functional in normal cells, the researchers harnessed its potential to inhibit the growth of p53-deficient cancer cells.

This paracrine effect was brought about by the tumor suppressor Par-4, which specifically kills cancer cells. Although other tumor suppressors exist, what makes Par-4 so special is that it is not mutated as frequently as other known suppressors, and it's "selective" in its actions in that Par-4 will only kill cancer cells and not normal cells. Importantly, it's secretion from normal cells can be induced by activating p53 so that Par-4 enters circulation, thereby potentially targeting at distant sites.

"As normal cells far outnumber the cancer cells in patients, we sought to empower the normal cells to trigger in p53-deficient ," said Rangnekar, associate director of transdisciplinary collaborations for the UK Markey Cancer Center. "Our findings have potential for targeting local, as well as metastatic tumors, and future studies will use FDA-approved drugs to induce Par-4 secretion."

Related Stories

Tipping the balance between senescence and proliferation

Nov 15, 2013

An arrest in cell proliferation, also referred to as cellular senescence, occurs as a natural result of aging and in response to cellular stress. Senescent cells accumulate with age and are associated with many aging phenotypes, ...

Biologists ID new cancer weakness

Nov 14, 2013

About half of all cancer patients have a mutation in a gene called p53, which allows tumors to survive and continue growing even after chemotherapy severely damages their DNA.

Recommended for you

Specific oxidation regulates cellular functions

1 hour ago

For a long time, hydrogen peroxide has been considered as a dangerous metabolite that can damage cells through oxidation. This, however, is not its only role in the cell. Scientists from the German Cancer Research Center ...

New disease mechanism discovered in lymphoma

1 hour ago

Programmed cell death is a mechanism that causes defective and potentially harmful cells to destroy themselves. It serves a number of purposes in the body, including the prevention of malignant tumor growth. ...

Researcher to cancer: 'Resistance will be futile'

9 hours ago

Turning the tables, Katherine Borden at the University of Montreal's Institute for Research in Immunology and Cancer (IRIC) has evoked Star Trek's Borg in her fight against the disease. "Cancer cells rapidly ...

How does prostate cancer form?

11 hours ago

Prostate cancer affects more than 23,000 men this year in the USA however the individual genes that initiate prostate cancer formation are poorly understood. Finding an enzyme that regulates this process ...

User comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.