Research Roundup: Promising New ALS Drug Candidates, Bee Venom Kills Cancer Cells and More
Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.
Honeybee Venom Kills Aggressive Breast Cancer Cells
Researchers from Herry Perkins Institute of Medical Research and The University of Western Australia tested the venom from 312 honeybees and bumblebees in Perth Western Australia, Ireland and England to determine its effect on clinical subtypes of breast cancer, including triple-negative breast cancer. Publishing their findings in the journal npj Precision Oncology, they demonstrated that the honeybee venom quickly destroyed triple-negative breast cancer and HER2-enriched breast cancer cells. The overall focus was on studying the anti-cancer properties of honeybee venom and specifically, a component of it, melittin, on different types of breast cancer cells.
“No one had previously compared the effects of honeybee venom or melittin across all of the different subtypes of breast cancer and normal cells,” said Ciara Duffy, who led the research. “We tested honeybee venom on normal breast cells, and cells from the clinical subtypes of breast cancer: hormone receptor positive, HER2-enriched, and triple-negative breast cancer. We tested a very small, positively charged peptide in honeybee venom called melittin, which we could reproduce synthetically, and found that the synthetic product mirrored the majority of the anti-cancer effects of honeybee venom.”
Duffy and the team found that a specific concentration of honeybee venom resulted in 100% cancer cell death, with minimal effects on normal cells. Duffy noted, “We found that melittin can completely destroy cancer cell membranes within 60 minutes.”
The melittin also significantly decreased the chemical messages of cancer cells that they require for growth and cell division—and within 20 minutes. Duffy noted, “We found that melittin can be used with small molecules or chemotherapies, such as docetaxel, to treat highly-aggressive types of breast cancer. The combination of melittin and docetaxel was extremely efficient in reducing tumor growth in mice.”
BMI Bigger Risk Factor for Diabetes than Genetics
A study out of the University of Cambridge, UK and University of Milan, Italy, of 445,765 people found that body mass index—in other words, bodyweight—was a bigger risk factor for diabetes than genetics. The data was from the UK Biobank and the average age was 57.2 years and 54% were women. Inherited risk of diabetes was evaluated using 6.9 million genes. Height and weight were measured to calculate BMI. They were then divided into five groups according to genetic risk. They were also split into five groups according to BMI. They were then followed until an average age of 65.2 years. In that period, 31,298 developed type 2 diabetes. The highest BMI group had an 11-fold increased risk of diabetes compared to the lowest BMI group, and they also had a greater likelihood of developing diabetes than all other BMI groups, regardless of genetic risk.
Compound Seems to Repair Neurological Damage
Researchers at the German Center for Neurodegenerative Diseases (DZNE), UK and Japan, created a neurologically acting protein and tested it in mice. The molecule decreased symptoms of certain neurological injuries and diseases. Also, on the microscopic level, it established and repaired neuronal connections. The molecule is called CPTX and the tests on mice were in models of Alzheimer’s disease, spinal cord injury and cerebellar ataxia, which is marked by a failure of muscle coordination. The molecule seemed to increase the ability of synapses to change, which is associated with memory formation, and elevated the synapses’ activity, and decreased the density of dendritic spines.
Genetic Mutations Possibly Linked to Infertility and Early Menopause
Investigators at Washington University School of Medicine identified a gene that appears to be associated with fertility. When missing in fruit flies, roundworms, zebrafish and mice, the animals are infertile or lose their fertility early. By analyzing genetic data in humans, the scientists discovered a link between mutations in this gene and early menopause. The gene is a nuclear envelope membrane protein 1 (NEMP1). In animals, mutations in the equivalent gene have been associated with eye development in the early embryos of fruit flies.
Promising New ALS Drug Candidates
Researchers from the University of Liverpool (UK) and the University of Nagoya (Japan) developed a Selenium-based molecule called beselen and several other novel compounds that appear to change the toxic qualities of superoxide dismutase (SOD1), a protein linked to some cases of amyotrophic lateral sclerosis (ALS). They published their research in the journal EBioMedicine.
ALS is a neurodegenerative disease that affects motor neurons and the neuronal links between the brain and muscles. As the disease progresses, the nerve links die and the patient becomes paralyzed, with the majority dying within two to five years after diagnosis. About 20% of the familial ALS cases are linked to dominant mutations in the sod1 gene. One of the known causes of the disease is aggregation of mutant SOD1 protein in familial cases and of wild-type SOD1 in some sporadic ALS cases. The only two drugs approved, both of which have limited benefits, are riluzole, approved in 1995, and edaravone, approved in 2017.
“The fact that this new generation of organo-selenium compounds have better in vitro neuroprotective activity than edaravone holds a significant promise for the potential of this class of compounds as an alternative therapeutic agent for ALS treatment,” said Samar Hasnain, who led the research team. “The ability of these compounds to target cysteine 111 in SOD may have wider therapeutic applications targeting cysteines of enzymes involved in pathogenic and viral diseases including the main protease of SARS-CoV-2.”
Koji Yamanaka, a physician-neuroscientist at Nagoya University, said, “it is very encouraging that a number of these novel Selenium compounds exhibited better in vitro neuroprotection in mouse neuronal cells than edaravone. In vivo disease onset delay by ebselen has been demonstrated for the first time in ALS mouse model and further improvement can be expected from the new novel compounds in view of their improved in vitro protection. Choices are very limited for a current ALS therapy, therefore, we are excited to take a significant step forward for developing a new class of drug candidates for ALS.”