Cancer cells have a notorious ability to multiply rapidly and spread easily throughout the body. One of the reasons they are so successful is their ability to undergo a process called epithelial-to-mesenchymal plasticity, which makes them resistant to elimination by anticancer therapies. In an effort to find new ways to combat this resistance, researchers have been searching for newer anticancer agents that can target these “rogue” cancer cells.

A team of scientists led by Dr. Hideyuki Saya, Director of the Oncology Innovation Center at Fujita Health University in Japan, has made a groundbreaking discovery about the potential of benzaldehyde to halt therapy-resistant pancreatic cancer. This sweet-smelling molecule is responsible for the aroma of almonds, apricots, and figs, but it also has potent anticancer properties.

The researchers were driven by a desire to uncover the mechanism behind benzaldehyde’s anticancer effects, particularly after learning that one of their colleagues had demonstrated its potential back in the 1980s. The first author of the study, Dr. Jun Saito, was motivated by her parents’ pioneering work on benzaldehyde and its derivatives.

The team conducted extensive research using a mouse model grafted with growing pancreatic cancer cells. They found that benzaldehyde inhibited the growth of these cancer cells, even when they had become resistant to radiation therapy and treatment with osimertinib, an agent blocking tyrosine kinases in growth factor signaling.

Their findings revealed that benzaldehyde exerts its anticancer effects by preventing interactions between a key signaling protein called 14-3-3ζ and histone H3. This interaction is crucial for cancer cell survival and treatment resistance. By blocking this interaction, benzaldehyde reduced the expression of genes related to epithelial-mesenchymal plasticity.

The study also showed that benzaldehyde synergized with radiation therapy to eliminate previously resistant cancer cells. Furthermore, a derivative of benzaldehyde was found to inhibit the growth of pancreatic tumors and suppress epithelial-to-mesenchymal plasticity, preventing metastasis.

Dr. Saya’s team believes that their results suggest that inhibition of the interaction between 14-3-3ζ and its client proteins by benzaldehyde has the potential to overcome the problem of therapy resistance. This study opens up possibilities for using benzaldehyde as a combinatorial anticancer agent, alongside molecular-targeted therapies.

The implications of this research are significant, offering new hope for patients with therapy-resistant pancreatic cancer. Further studies will be necessary to confirm these findings and explore their potential applications in the clinic.

The scientific community has made another groundbreaking discovery that reveals how our beloved morning coffee might be doing more than just waking us up. A recent study conducted by researchers at Queen Mary University of London’s Cenfre for Molecular Cell Biology sheds light on the potential anti-ageing properties of caffeine, the world’s most popular neuroactive compound.

The research, published in the journal Microbial Cell, delves into the intricate mechanisms within our cells and how they respond to stress and nutrient availability. The scientists used a single-celled organism called fission yeast as a model to understand how caffeine affects ageing at a cellular level.

One of the key findings was that caffeine doesn’t act directly on the growth regulator called TOR (Target of Rapamycin), which is responsible for controlling energy and stress responses in living things for over 500 million years. Instead, it works by activating another crucial system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.

“When your cells are low on energy, AMPK kicks in to help them cope,” explains Dr Charalampos (Babis) Rallis, Reader in Genetics, Genomics, and Fundamental Cell Biology at Queen Mary University of London, the study’s senior author. “And our results show that caffeine helps flip that switch.”

The implications of this discovery are significant, as AMPK is also the target of metformin, a common diabetes drug being studied for its potential to extend human lifespan together with rapamycin. The researchers demonstrated using their yeast model that caffeine’s effect on AMPK influences how cells grow, repair their DNA, and respond to stress – all of which are tied to ageing and disease.

These findings open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines. So, the next time you reach for your coffee, remember that it might be doing more than just boosting your focus – it could also be giving your cells a helping hand in slowing down your ageing process.

The skin serves as our body’s first line of defense against external threats. As we age, however, the epidermis – the outermost layer of skin – gradually becomes thinner and loses its protective strength. Research has long emphasized the benefits of vitamin C (VC) in maintaining skin health and promoting antioxidant properties.

Recently, a team of researchers in Japan made an exciting discovery: VC helps thicken the skin by directly activating genes that control skin cell growth and development. Their findings, published online in the Journal of Investigative Dermatology, suggest that VC may restore skin function by reactivating genes essential for epidermal renewal.

Led by Dr. Akihito Ishigami, Vice President of the Division of Biology and Medical Sciences at Tokyo Metropolitan Institute for Geriatrics and Gerontology, the study used human epidermal equivalents – laboratory-grown models that closely mimic real human skin. In this model, skin cells are exposed to air on the surface while being nourished from underneath by a liquid nutrient medium.

The researchers applied VC at concentrations comparable to those typically transported from the bloodstream into the epidermis and found that VC-treated skin showed a thicker epidermal cell layer without significantly affecting the stratum corneum (the outer layer composed of dead cells) on day seven. By day 14, the inner layer was even thicker, and the outer layer was found to be thinner, suggesting that VC promotes the formation and division of keratinocytes.

Importantly, the study revealed that VC helps skin cells grow by reactivating genes associated with cell proliferation. This process occurs through DNA demethylation – a process in which methyl groups are removed from DNA, allowing for gene expression and promoting cell growth.

The researchers further identified over 10,138 hypomethylated differentially methylated regions in VC-treated skin and observed a 1.6- to 75.2-fold increase in the expression of 12 key proliferation-related genes. When a TET enzyme inhibitor was applied, these effects were reversed, confirming that VC functions through TET-mediated DNA demethylation.

These findings reveal how VC promotes skin renewal by triggering genetic pathways involved in growth and repair. This suggests that VC may be particularly helpful for older adults or those with damaged or thinning skin, boosting the skin’s natural capacity to regenerate and strengthen itself.

“We found that VC helps thicken the skin by encouraging keratinocyte proliferation through DNA demethylation, making it a promising treatment for thinning skin, especially in older adults,” concludes Dr. Ishigami.

This study was supported by grants from the Japan Society for the Promotion of Science (JSPS) KAKENHI: grant number 19K05902.