New Research Shows How CBD May Kill Breast Cancer Cells

 

We’ve heard that cannabidiol (CBD) benefits cancer patients in many ways. The second-most prominent cannabinoid in cannabis sativa has been shown to reduce pain, shrink tumors, and relieve symptoms of chemotherapy. While previous research suggests that CBD prevents the growth of cancerous tumors by promoting apoptosis, or programmed cell death, we’re only just beginning to understand how that occurs.

 

A recent research paper, “Novel mechanism of cannabidiol-induced apoptosis in breast cancer cell lines” by Sultan et al. from the Alexandria University in Egypt, not only proposes CBD as a useful treatment for certain types of breast cancer, it explores the molecular mechanism of antitumor activity in this formerly overshadowed cannabinoid.

 

 

Three Subtypes of Breast Cancer

 

Before we discuss this study’s significance, let’s briefly cover some breast cancer basics. There are three main subtypes:

• Hormone receptor-positive
• Human epidermal growth factor receptor two (HER2) positive
• Triple-negative

 

Hormone receptor-positive means the breast cancer tumor contains receptors for either of the female sex hormones, estrogen or progesterone. The most common form of breast cancer, hormone receptor-positive, accounts for about 65% of all cases.

 

Then we have HER2 positive cases, which involve a genetic mutation in the HER2 receptor. This receptor is in charge of cell division and growth in the breast. The mutation causes the body to make too many HER2 proteins, resulting in uncontrolled growth of breast cells. About 20% of breast cancer patients have the HER2 positive type, which can also be hormone receptor-negative or hormone receptor-positive. Typically, HER2 positive cases of breast cancer test negative for estrogen and progesterone receptors.

 

Lastly, triple-negative breast cancer is the least common and most aggressive form among these three subtypes. Triple-negative breast cancer gets its name from the fact that it lacks receptors for estrogen, progesterone, and HER2. Only about 15% of breast cancer patients have this type.

 

Why is the lack of these receptors distressing? When it comes to breast cancer treatment, hormone receptor-positive and HER2 positive types currently have more options. When scientists can identify receptors that lead to tumor growth, they can develop prescription drugs to target those receptors.

 

Treatment for hormone receptor-positive breast cancer may include medications that block hormone communication or reduce estrogen production. Similarly, drugs that specifically target HER2 receptors, such as trastuzumab, are an option for women with HER2 positive breast cancer.

 

On the other hand, women with early-stage triple-negative breast cancer have fewer treatment options and usually need chemotherapy. This makes the triple-negative type particularly interesting to scientists in search of novel treatments and medications.

 

Now that we understand the foundations of breast cancer types and treatments, let’s examine the exciting discoveries this study reveals!

 

Shattering the Cellular DNA of Cancer Cells

 

Previous studies suggest that CBD induces apoptosis (cell death) in cancer cells through the human body’s naturally occurring cannabinoid receptors, as well as through our vanilloid receptors – the molecular gateway to our pain pathway. Expanding on this knowledge, Sultan and colleagues focused on how CBD affects two populations of breast cancer cells: estrogen receptor-positive (ER-positive) subtype, T-47D, and another triple negative subtype, MDA-MB-231.

 

You’d think scientists could come up with better names, right?

 

But Sultan et al. didn’t choose these populations based on snazzy names. Known as “immortalized cell lines,” these two populations grow indefinitely in culture dishes, providing researchers with a continuously dividing supply of cancerous cells to work on.

 

The researchers found that adding CBD in a dose-dependent manner causes both cell lines to undergo significant structural changes that inhibit cell survival and activate apoptosis.

 

In English, that means the more CBD you add to these two populations of breast cancer cells, the more the cells shrivel up and die. But the cancer cells don’t simply die; their cellular DNA shatters into fragments. Their mitochondria, or energy powerhouses, cease to function. Eventually, your body recognizes these broken shreds of cancer as cellular garbage and promptly disposes of them. Basically, CBD is like Godzilla, totally crushing the most common and most difficult-to-treat cancer cells.  

 

Now that you have the visual of a giant reptilian monster squashing cancer cells like buildings in a single stomp, the non-fiction piece of this story gets even better.

 

Cancer Cell Destruction and Tumor Shrinkage

 

In this 2018 study, Sultan et al. go on to describe the underlying mechanisms behind this cancer-killing monster. To do this, they examine three key players in cancer development:

• Mammalian target of rapamycin (mTOR): involved in regulating cell growth, proliferation, and survival
• Cyclin D1: a protein that causes a cell to start copying its DNA in preparation to divide
• Peroxisome proliferator-activated receptor gamma (PPARγ): a ligand-binding transcription factor that plays a role in cellular proliferation and apoptosis

 

Before I lose you, let’s break this down.

 

Overstimulation of the mTOR pathway can cause cells to grow and divide out of control. This may then initiate tumor development in many parts of the body, including the breast.

 

Additionally, overstimulation of the mTOR pathway leads to overexpression of cyclin D1, which ultimately causes uncontrolled cell division.

 

Lastly, PPARγ is a transcription factor, meaning it’s a protein that can bind to DNA and regulate gene expression. PPARγ has been found to reduce the growth rate and malignancy of breast cancer cells, making it the sole factor we want to see more of out of these three.

 

So how does CBD affect mTOR, cyclin D1, and PPARγ in these two breast cancer cell lines?

 

Remember, PPARγ is a ligand-binding transcription factor. CBD is the ligand it binds to. This CBD-PPARγ complex suppresses mTOR expression along with the downstream production of cyclin D1. When cyclin D1 activity declines, PPARγ activity increases even more, leading to the destruction of cancer cells and shrinkage of tumors.

 

Importance of Scientific Research

 

Not only does this study at the Egyptian university propose CBD as a beneficial treatment for two subtypes of breast cancer – one that accounts for about 65% of cases and the other particularly difficult to treat – it demonstrates the importance of scientific research on the medical applications of cannabis.

 

But cannabis research is no easy feat; major regulatory roadblocks must be overcome. For example, cannabis remains illegal at the federal level, where it’s listed as a Schedule 1 drug. In order for an organization to conduct research, it must submit an application to the DEA, requesting a special license to work with Schedule 1 substances – a process that can take a year or longer (filled with intimidating hurdles).

 

Even with the DEA’s permission, researchers can only study cannabis from one authorized provider known as “the farm” at the University of Mississippi. This provider grows specific strains under contract with the National Institute on Drug About – not quite the caliber of cannabis we see in the marketplace.

 

Despite these challenges, scientists are moving forward with new cannabis research projects at the University of California, Los Angeles (UCLA), the University of California, Irvine (UCI) and the University of California, San Diego (UCSD), to name a few. When there’s a will, there’s a way.

 

If you have any questions about this article or want to learn more about cannabis as a cancer treatment, head over to Nugg’s Cannabis Concierge. Our expert team is happy to answer any cannabis-related questions you have.