UCLA scientists show new tumor-suppressor gene can reduce cervical cancer growth

Human papillomavirus--Courtesy of Laboratory of Tumor Virus Biology

University of California, Los Angeles, scientists have discovered a protein known as cystatin E/M and identified its involvement in the growth of cervical cancer. They say that the protein can prevent cellular inflammation, which is known to accelerate cancer growth. The findings may point to new directions for cancer treatment.

Dr. Eri Srivatsan and colleagues at the UCLA Jonsson Comprehensive Cancer Center published their work in the journal Molecular and Cellular Biology.

Cervical cancer develops after a woman contracts the human papillomavirus (HPV), the most common sexually transmitted disease, with environmental factors like smoking increasing the likelihood of developing the cancer. Cervical cancer represents the second most common cause of cancer-related deaths in women worldwide, and in the U.S., HPV is detected in 90% of cervical cancer tumors.


Like this story? Subscribe to FierceBiotech!

Biopharma is a fast-growing world where big ideas come along every day. Our subscribers rely on FierceBiotech as their must-read source for the latest news, analysis and data in the world of biotech and pharma R&D. Sign up today to get biotech news and updates delivered to your inbox and read on the go.

Srivatsan and his team showed that cystatin E/M--previously characterized in primary tumors by his group and others--prevents a transcription factor called nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) from entering the nucleus of cervical cancer cells, binding to genes and causing their activation.

Because NF-κB is well known to regulate cellular inflammation, the identification of cystatin E/M in negatively regulating inflammation in cervical cancer cells could have significant importance.

"When key inhibitory mechanisms break down, cancer cells produce inflammation that helps fuel cancer cell growth," said Srivatsan in a release. "By identifying this protein, we have discovered a key regulator of this breakdown. This is the first time we have found that inhibition of the protein kinase by cystatin E/M plays a regulatory role in cell inflammation."

Building on previous findings, the team studied 20,000 genes in two cell lines and analyzed 66 samples of normal and cervical tissue samples to deduce the function of cystatin E/M. Using a genetic system in mice prone to develop tumors, they confirmed that activating cystatin E/M suppresses tumor growth by preventing NF-κB translocation to the nucleus--ultimately showing that cystatin E/M can act as a tumor-suppressor gene.

The team will begin to determine the function of cystatin E/M to inhibit other types of cancers such as chemo- and radiation-resistant breast cancers.

- here’s the release
- and the journal abstract


Suggested Articles

Brigham and Women’s Hospital scientists linked a noncoding RNA to atherosclerosis in a discovery that could aid in the development of new heart drugs.

Researchers discovered that inactivating a subtype of the protein beta-arrestin-2 in mice restored the ability of the brain to dispose of toxic tau.

A newfound link between BMAL1, a protein involved in circadian rhythms, and triple-negative breast cancer could point to new treatment strategies.