Enhancing Breast Cancer Treatment in Mice: The Impact of Reducing Vitamin B5 on Cancer Growth This title effectively captures the essence of the article while emphasizing the potential implications for improving breast cancer treatment methods

Vitamin B5 Found To Fuel Breast Cancer growth, New Study Reveals

September 13, 2025

A groundbreaking investigation spearheaded by scientists at the Francis Crick Institute, in collaboration with the National Physical Laboratory (NPL) and Imperial College London, has uncovered a critical dependency of aggressive breast cancer cells on vitamin B5 for growth and survival.This discovery, stemming from the Cancer Grand Challenges team Rosetta, funded by Cancer Research UK, could revolutionize approaches to combating the disease.

The Role of Myc in Cancer Metabolism

The study, published in Nature Metabolism, focused on the metabolic impact of Myc, a gene frequently overexpressed in various cancers. Researchers found that high levels of Myc disrupt normal cellular processes, accelerate cell growth, and render tumor cells notably reliant on specific nutrients.Identifying and targeting these dependencies presents a promising therapeutic strategy, though complex due to varying Myc expression within tumors.

Innovative Imaging Techniques Uncover the Link

To overcome this challenge,researchers developed a unique model using mice with tumors exhibiting both high and low Myc levels. They also transplanted human breast cancer tissue into mice, creating a similar mosaic of Myc expression. Utilizing advanced mass spectrometry imaging, they observed a strong correlation between vitamin B5 concentration and areas of high Myc activity in both mouse and human tumor samples-a correlation consistently observed in patient biopsies.

How Vitamin B5 supports cancer Cell Growth

The research demonstrated that Myc increases the production of a transporter protein, facilitating increased vitamin B5 uptake into cells. Artificially boosting the production of this transporter in cells with low Myc levels was sufficient to stimulate growth, mimicking the effect of high Myc expression. This highlights the crucial role vitamin B5 plays in fueling cancer cell proliferation.

Vitamin Restriction Slows Tumor Growth

further experiments involved feeding mice a diet deficient in vitamin B5. Remarkably, tumors-both those with high and low Myc expression-grew considerably slower compared to mice on a standard diet. This effect was also replicated in the transplanted human breast cancer tissue.

Vitamin B5 and Cellular Energy Production

Scientists believe Vitamin B5’s impact on tumor growth stems from its essential role in cellular metabolism. Once inside cells, it transforms into coenzyme A, a vital component in numerous metabolic pathways that generate energy and produce essential building blocks like fats, proteins, and carbohydrates-all critical for cell growth.

A Nuanced Approach to Cancer Treatment

While the findings establish a connection between vitamin B5 and cancer growth, researchers caution against simply restricting vitamin intake. Vitamins are essential for a healthy immune system, which plays a crucial role in fighting cancer. The focus now is on developing strategies to selectively target and weaken tumors without compromising immune function.

Ongoing Research and Biomarker Potential

Researchers are also exploring vitamin B5 levels as a potential biomarker to assess a tumor’s genetic makeup and predict its responsiveness to Myc-targeted therapies. Collaborations with King’s College London are underway to develop tracers for vitamin B5 that could identify patients most likely to benefit from specific treatments.

Did You Know? According to the national cancer Institute, breast cancer is the most common cancer in American women, except for skin cancers. Early detection and advancements in treatment have led to increased survival rates, but new therapeutic strategies are always needed.

Pro Tip: Maintaining a balanced diet with adequate vitamin intake is crucial for overall health, but it’s essential to consult with a healthcare professional before making important dietary changes, especially during cancer treatment.

gene	Role	Impact on Vitamin B5
Myc	drives cell growth and metabolism	Increases vitamin B5 transporter production
Vitamin B5 Transporter	Facilitates vitamin B5 uptake	Increased expression leads to faster cell growth

Understanding Metabolic Dependencies in Cancer

The concept of metabolic dependencies in cancer is gaining increasing attention.Cancer cells often exhibit altered metabolic pathways compared to normal cells, making them vulnerable to targeting specific metabolic processes. The discovery of vitamin B5’s role in breast cancer is a prime exmaple of how understanding these dependencies can lead to novel therapeutic strategies.

Research into cancer metabolism is ongoing, and future studies will likely identify other essential nutrients or metabolic pathways that cancer cells rely on. This could pave the way for personalized cancer treatments tailored to the specific metabolic profile of each patient’s tumor.

Frequently Asked Questions About Vitamin B5 and Cancer

• What is the role of vitamin B5 in cancer growth? Vitamin B5 is essential for converting nutrients into energy, and cancer cells utilize this process to rapidly proliferate.
• Should cancer patients avoid vitamin B5? Restricting vitamin B5 intake is not currently recommended, as it is indeed vital for immune function. Researchers are focused on selective targeting of tumors.
• How was the link between vitamin B5 and cancer discovered? Advanced mass spectrometry imaging revealed a correlation between vitamin B5 concentration and areas of high Myc activity in tumors.
• What is the Myc gene? myc is a gene that promotes cell growth. Overexpression of this gene is common in many cancers.
• Will this discovery lead to new cancer treatments? Researchers are developing strategies to selectively weaken tumors by disrupting their vitamin B5 supply, without impacting healthy cells.

What are your thoughts on this new discovery? Share your comments below!

How does upregulating pantothenate kinase (PANK) in breast cancer cells contribute to their metabolic reprogramming?

Enhancing Breast Cancer Treatment in Mice: The impact of Reducing Vitamin B5 on Cancer Growth

The Metabolic Vulnerability of Breast Cancer Cells

Breast cancer, a complex disease with diverse subtypes, continues to be a important global health challenge. Current treatment strategies – including chemotherapy, radiation, adn hormone therapy – often face limitations due to drug resistance and debilitating side effects. Emerging research focuses on exploiting metabolic vulnerabilities within cancer cells to enhance treatment efficacy. One promising area investigates the role of pantothenic acid, commonly known as Vitamin B5, in fueling breast cancer progression. This article details how reducing Vitamin B5 availability impacts tumor growth in murine models, offering potential avenues for improved breast cancer therapies.

Vitamin B5 and Coenzyme A (CoA) Synthesis: A Critical Link

Vitamin B5 is a crucial precursor for Coenzyme A (CoA), a vital cofactor involved in numerous metabolic pathways, including fatty acid metabolism, glucose oxidation, and amino acid catabolism. Cancer cells exhibit altered metabolic profiles, often relying heavily on these pathways to support their rapid proliferation and survival.

* Increased CoA Demand: Breast cancer cells, particularly aggressive subtypes, demonstrate an elevated demand for CoA to synthesize lipids for membrane production and energy storage.

* Pantothenate Kinase (PANK) Upregulation: Many breast cancer cells upregulate pantothenate kinase (PANK), the enzyme responsible for the first step in CoA synthesis, further increasing their reliance on Vitamin B5.

* Metabolic Reprogramming: This metabolic reprogramming creates a dependency on external Vitamin B5 sources, making it a potential therapeutic target.

Preclinical Studies: reducing Vitamin B5 in Murine Breast Cancer Models

Several preclinical studies utilizing murine models of breast cancer have demonstrated the efficacy of Vitamin B5 restriction or PANK inhibition in suppressing tumor growth.

Impact on Tumor Growth and Metastasis

* Dietary Restriction: Studies involving a Vitamin B5-deficient diet in mice bearing xenografted breast cancer tumors showed significant reductions in tumor volume and decreased metastatic spread. This suggests that limiting external Vitamin B5 availability can disrupt cancer cell metabolism.

* PANK Inhibitors: Researchers have developed specific PANK inhibitors that block CoA synthesis. Administration of these inhibitors to mice with breast cancer resulted in:

* Reduced tumor growth rates.

* Decreased cell proliferation.

* Increased apoptosis (programmed cell death) in tumor cells.

* Suppression of metastasis to distant organs.

* Synergistic Effects with Chemotherapy: Combining PANK inhibitors with conventional chemotherapy agents (like paclitaxel or doxorubicin) exhibited synergistic anti-tumor effects in murine models.This indicates that Vitamin B5 pathway inhibition can enhance the sensitivity of cancer cells to existing treatments.

Specific Breast Cancer Subtypes & Response

The response to Vitamin B5 restriction or PANK inhibition varies depending on the breast cancer subtype:

* Triple-Negative Breast Cancer (TNBC): TNBC, known for its aggressive nature and limited treatment options, appears particularly sensitive to Vitamin B5 pathway disruption. This is likely due to its high metabolic rate and reliance on fatty acid synthesis.

* HER2-Positive Breast Cancer: While showing some response, HER2-positive tumors may require higher doses of PANK inhibitors or combination therapies to achieve significant growth inhibition.

* Hormone Receptor-positive Breast Cancer: The impact on hormone receptor-positive tumors is still under investigation, but preliminary data suggests that Vitamin B5 pathway inhibition can modulate hormone signaling pathways.

Mechanisms of Action: How Vitamin B5 Reduction Impacts Cancer Cells

The anti-cancer effects of Vitamin B5 restriction are multifaceted:

1. CoA Depletion: Reducing Vitamin B5 availability directly leads to a decrease in intracellular CoA levels, disrupting essential metabolic processes.
2. Fatty Acid Synthesis Inhibition: CoA is crucial for fatty acid synthesis. Inhibiting CoA production impairs the ability of cancer cells to generate lipids needed for membrane formation and energy storage.
3. Mitochondrial Dysfunction: Disruption of CoA metabolism affects mitochondrial function, leading to decreased ATP production and increased oxidative stress.
4. Cell Cycle Arrest: Vitamin B5 reduction can induce cell cycle arrest, preventing cancer cells from dividing and proliferating.
5. Enhanced Autophagy: In some cases, Vitamin B5 restriction triggers autophagy, a cellular self-eating process that can eliminate damaged organelles and proteins, contributing to cancer cell death.

Benefits of Targeting Vitamin B5 in Breast Cancer Treatment

* Novel Therapeutic Strategy: Offers a new approach to breast cancer treatment, perhaps overcoming drug resistance.

* Targeted Approach: Exploits a metabolic vulnerability specific to cancer cells, minimizing harm to healthy tissues.

* Synergistic Potential: Enhances the efficacy of existing chemotherapy regimens.

* Potential for Personalized Medicine: Identifying patients with high PANK expression could predict responsiveness to Vitamin B5 pathway inhibitors.

Practical Considerations & Future Directions

While promising, translating these findings from murine models to human clinical