Feinberg
Northwestern Medicine | Northwestern University | Faculty Profiles

News Center

  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
    • Podcast
  • Press Release
  • Media Coverage
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Menu
  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
    • Podcast
  • Press Release
  • Media Coverage
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Home » Study Pinpoints New Targets for Ovarian Cancer Treatment
Uncategorized

Study Pinpoints New Targets for Ovarian Cancer Treatment

By medwebDec 26, 2012
Share
Facebook Twitter Email
Marcus Peter, PhD, professor of hematology/oncology, is the co-lead author of a paper showing how ovarian cancer cells change the normal cells around them into versions that promote tumor growth.

Unraveling the mechanism that ovarian cancer cells use to change normal cells around them into cells that promote tumor growth has identified several new targets for treatment of this deadly disease.

In the December issue of the American Association for Cancer Research journal Cancer Discovery, a team or researchers from Northwestern University Feinberg School of Medicine and the University of Chicago Medicine show that ovarian cancer cells induce nearby cells to alter their production of three microRNAs – small strands of genetic material that are important regulators of gene expression.

By changing gene expression, microRNAs can modify a cell’s function. In this case, they convert normal, healthy fibroblasts into cancer-associated fibroblasts (CAFs). These CAFs pump out chemical signals telling cancer cells to multiply, invade healthy tissues, and travel to distant sites in the abdomen. Importantly, by reversing the microRNA signals the researchers were able to cause CAFs to revert to normal fibroblasts.

“Only a few years ago scientists learned how to reprogram normal cells into cells that can give rise to any cell type in the body,” said Marcus Peter, PhD, professor of hematology/oncology, and one of the lead authors on the study. “Our work demonstrates that cancer cells also have the ability to reprogram cells in their environment into cells that support their growth and that this process involves microRNAs.”

Fibroblasts are the primary cellular component of connective tissue. They provide the structural framework for other tissues and aid in wound healing. When fibroblast-dense tissues are infiltrated by cancer cells, however, intimate cross-talk between fibroblasts and cancer cells can convert them to cancer-associated fibroblasts, shifting them into a new role.

“These cancer-supporting cells provide a novel and appealing treatment target,” said Ernst Lengyel, MD, PhD, professor of obstetrics and gynecology at the University of Chicago, and the second lead author on the study. “Cancer cells mutate rapidly, which enables them to develop drug resistance. But cancer-associated fibroblasts are genetically stable,” he said. “Their harmful behavior is driven by the microRNAs. Inhibiting those signals is a new way to fight this disease. It disrupts the cancer’s support system and is unlikely to evolve resistance.”

The researchers found that cancer cells caused normal fibroblasts to reduce production of two microRNAs, miR-31 and miR-214, and to increase production of miR-155. Since microRNAs usually block gene expression, reduced levels increased expression of several of their target genes. Many of those genes are involved in the production of the chemical signals associated with CAFs.

The most highly upregulated such signal, known as CCL5, is a “key tumor-promoting factor,” the authors show. When human ovarian cancer cells and CAFs were co-injected into mice, the tumor cells soon replaced normal ovarian structures. Antibodies that neutralized CCL5 inhibited this augmented growth.

“One strength of our study is that we used tumor cells and CAFs from patients, rather than cell lines,” said Lengyel. “Our model system is as close as possible to the real situation.”

“Therapeutic approaches targeting microRNAs in cancer cells are under development,” added Peter. “Our work suggests that it might be possible to modify microRNA expression in cancer-associated fibroblasts for therapeutic benefit.”

Research
Share. Facebook Twitter Email

Related Posts

Hospitals Bound to Patient Safety Rules that Aren’t all Backed by Evidence

Jun 24, 2022

Identifying Protein Interactions that Promote Cancer Growth

Jun 24, 2022

Calcium Channel Blockers May Improve Chemotherapy Response

Jun 21, 2022

Comments are closed.

Latest News

Student Spearheads Ukraine Aid Efforts

Jun 27, 2022

Hospitals Bound to Patient Safety Rules that Aren’t all Backed by Evidence

Jun 24, 2022

Identifying Protein Interactions that Promote Cancer Growth

Jun 24, 2022

Combination Treatment May Improve Quality of Life in Kidney Cancer

Jun 23, 2022

Calcium Channel Blockers May Improve Chemotherapy Response

Jun 21, 2022
  • News Center Home
  • Categories
  • Press Release
  • Media Coverage
  • Editor’s Picks
  • News Archives
  • About Us
Flickr Photos
pride7
pride6
pride5
pride4
pride3
pride2
pride1
20220607_Feinberg Campus_0070
20220607_Feinberg Campus_0066
20220607_Feinberg Campus_0054
Northwestern University 2022. Photo by Jim Prisching
20220607_Feinberg Campus_0077

Northwestern University logo

Northwestern University Feinberg School of Medicine

RSS Facebook Twitter LinkedIn Flickr YouTube Instagram
Copyright © 2022 Northwestern University
  • Contact Northwestern University
  • Disclaimer
  • Campus Emergency Information
  • Policy Statements

Type above and press Enter to search. Press Esc to cancel.