Researchers identify a crucial protein that commands a key communications hub determining cell growth

January 3, 2018, National University of Singapore
Researchers identify a crucial protein that commands a key communications hub determining cell growth
A cell image showing the precise compartment called endosome (some are shown in arrows) where BPGAP1 interacts with its partner proteins to execute growth signaling. Credit: National University of Singapore

National University of Singapore biologists have identified a crucial protein that commands a key communications hub which determines cell growth.

Various proteins control key physiological functions when their activities are properly regulated. However, the same set of proteins could lead to undesirable outcomes if their amounts are at abnormal levels or their cell-to-cell communications are short-circuited. Two cell signalling pathways, the RAS/MEK and JNK pathways (named after distinct proteins that play crucial roles in controlling cell growth and cell death, respectively) are well-known to influence the way grow, divide or even commit suicide. Although various studies have shown that these two pathways can work in parallel or together to control cell fates, it is not clear how they influence or work with each other to promote cell proliferation, which can sometimes prime cells towards uncontrolled growth in cancers.

A team of researchers led by Prof Boon Chuan LOW from the Department of Biological Sciences, NUS has identified BPGAP1 as the key scaffold protein that is responsible for linking these two major signalling pathways together. This protein acts like a switch controlling the genetic programming for . When this is functioning properly, the two pathways can communicate with each other to maintain a balance in cell numbers. If it malfunctions, it could lead to uncontrolled growth of cells, causing cancer development. The team has also established the crucial steps involved in this precise activation mechanism at the cellular and molecular levels.

"The abnormal activation of certain proteins (epidermal growth factor receptor, RAS, MEK and JNK) are known to be associated with different ways of causing cancers. The identification of BPGAP1 represents a new one-stop hub that controls these activities. This opens the way for developing potential new therapeutics that could prevent tumour ," said Prof Low, who is also a Senior Principal Investigator at the Mechanobiology Institute, NUS.

The group plans to further delineate the precise sites and structure of the interaction between BPGAP1 and the JNK and MEK proteins, so as to pinpoint the most desirable sites on the molecule for the development of anti-cancer therapeutics.

Explore further: Disrupting cell signals may lead to new cancer treatments

More information: T Jiang et al. BPGAP1 spatially integrates JNK/ERK signaling crosstalk in oncogenesis, Oncogene (2017). DOI: 10.1038/onc.2016.466

Related Stories

Disrupting cell signals may lead to new cancer treatments

April 29, 2013
(Medical Xpress)—Scientists have taken a major step towards developing new treatments for certain cancers by disrupting the internal cellular signals that lead to the uncontrolled growth of cancerous cells.

Mechanobiology provides insight into disease and healing processes

March 19, 2015
Researchers in Singapore are gaining further insight into how the mechanical environment of cells drives fundamental cellular processes such as motility, growth and survival. These processes are integral to many clinical ...

New approaches to cell study contributes to cancer research

September 12, 2014
At Ryerson, some of our top researchers are committed to finding out how cells function, and to building our knowledge of the basic science of cellular function while investigating diseases and the potential for new therapies ...

Plant flavonoid luteolin blocks cell signaling pathways in colon cancer cells

January 23, 2012
Plant flavonoid luteolin blocks cell signaling pathways in colon cancer cells

Finding new cancer drugs in the neighborhood

January 24, 2017
Cancer is caused by an accumulation of genetic changes in a cell, that overcome the normal checks and balances leading to uncontrolled growth. A complex, interacting network of proteins controls all of a cell's processes, ...

Recommended for you

Dying cancer cells make remaining glioblastoma cells more aggressive and therapy-resistant

June 21, 2018
A surprising form of cell-to-cell communication in glioblastoma promotes global changes in recipient cells, including aggressiveness, motility, and resistance to radiation or chemotherapy.

Existing treatment could be used for common 'untreatable' form of lung cancer

June 21, 2018
A cancer treatment already approved for use in certain types of cancer has been found to block cell growth in a common form of lung cancer for which there is currently no specific treatment available.

Novel therapy makes oxidative stress deadly to cancer

June 21, 2018
Oxidative stress can help tumors thrive, but one way novel cancer treatments work is by pushing levels to the point where it instead helps them die, scientists report.

Researchers uncover new target to stop cancer growth

June 21, 2018
Researchers at the University of Wisconsin-Madison have discovered that a protein called Munc13-4 helps cancer cells secrete large numbers of exosomes—tiny, membrane-bound packages containing proteins and RNAs that stimulate ...

New treatment helps avoid deafness in child chemotherapy patients

June 21, 2018
An international trial has found that a medicine commonly used to treat poisoning is effective in reducing deafness in children receiving chemotherapy for cancer.

Higher body fat linked to lower breast cancer risk in younger women

June 21, 2018
While obesity has been shown to increase breast cancer risk in postmenopausal women, a large-scale study co-led by a University of North Carolina Lineberger Comprehensive Cancer Center researcher found the opposite is true ...

0 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.