Researchers propose 'brand new' way of investigating cancer's spread

By Paul Mayne
April 25, 2013

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KissPaul Mayne, Western News
Graduate student Donna Cvetkovic and Schulich School of Medicine & Dentistry professor Moshmi Bhattacharya are working toward a potential new method in addressing the metastasis of breast cancer.

 

Western researchers may have found another in-road into one day stopping the metastasis (spread) of breast cancer, by targeting the kisspeptin receptor protein (KISS1R), which binds kisspeptins - products of the KISS1 gene.

In many cancers, such as melanoma, ovarian, thyroid, gastric, lung and bladder cancers, the KISS1 gene acts as a metastasis-suppressor gene. However, in human breast tumours, there is an increase in KISS1 and KISS1R gene levels that correlates with higher tumour grade, increased metastatic potential and poor patient survival.

In a recently published paper in the online edition of the prestigious journal Endocrinology (April 2013), Schulich School of Medicine & Dentistry professor Dr. Moshmi Bhattacharya (Department of Physiology and Pharmacology, and Oncology) has shown KISS1R directly triggers breast cancer cell invasion, a key step in the metastasis process.

For the first time, this study shows KISS1R only stimulates invasion of breast cancer cells that are missing the estrogen receptor, a clinical target for hormonal breast cancer therapy.

“Typically one of the ways that breast cancers are classified is being estrogen receptor-positive or estrogen receptor-negative, and breast cancer cells that have lost their estrogen receptor are more aggressive. We found that kisspeptin significantly increased invasiveness of estrogen receptor-negative breast cancer cells,” said Donna Cvetkovic, a graduate student of Bhattacharya and lead author on the paper.

“However, in cells that still express estrogen receptor, stimulation with kisspeptin does not lead to invasion. So we believe estrogen receptor is acting as a brake, and when patients lose their estrogen receptor it allows KISS1R to signal and behave in a non-typical fashion.”

“The mechanism by which kisspeptin/KISS1R regulates breast cancer cell migration and invasion, two processes required for cancer metastasis, remain largely undefined,” added Bhattacharya, who is supported by a grant from the Canadian Institutes of Health Research. “In our earlier study we showed that KISS1R cross-talks with another receptor protein called the epidermal growth factor receptor (EGFR). EGFR is a growth stimulus protein that produces a more aggressive disease.”

Bhattacharya said while EGFR is targeted for breast cancer therapy, many patients develop resistance to the therapy. Since KISS1R talks with EGFR, this research raises the possibility of new treatment strategies, such as targeting both receptors to achieve a better therapeutic effect.

“We’re hoping to open the door to say it’s important that we look at the KISS1R receptor clinically as well, and not just the EGFR, leading perhaps in the future, combinational therapy,” she said.

However, Bhattacharya added there are several questions that remain to be answered.

“For example, what is the mechanism behind KISS1R-EGFR talking to each other? What is the mechanism by which the estrogen receptor controls the KISS1R? How does KISS1R stimulate breast cancer migration and invasion? It’s all brand new. We believe these only to be the tip of the iceberg.”























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