PEPTIDE FROM COW’S MILK KILLS STOMACH CANCER CELLS
Posted in News, Science & Research, Cancer, Immunity, Immune Health, Dairy, Dairy Ingredients
PHILADELPHIA—A peptide fragment derived from cow’s milk, known as lactoferricin B25 (LFcinB25), induces cell death of stomach cancer cells in culture, according to a new study published in the Journal of Dairy Science. The findings may lead to the future use of the peptide fragment as a potential therapeutic agent for gastric cancer.
“Gastric cancer is one of the most common causes of cancer-related mortality worldwide, especially in Asian countries," said Wei-Jung Chen, PhD, of the department of biotechnology and animal science of National Ilan University, Taiwan. “In general, the main curative therapies for gastric cancer are surgery and chemotherapy, which are generally only successful if the cancer is diagnosed at an early stage. Novel treatment strategies to improve prognosis are urgently needed."
Researchers evaluated the effects of three peptide fragments derived from lactoferricin B, a peptide in milk that has antimicrobial properties. Only one of the fragments, LFcinB25 reduced the survival of human AGS (Gastric Adenocarcinoma) cells in a dose-dependent and time-dependent manner.
Under a microscope the researchers could see that after one hour of exposure to the gastric cancer cells, LFcinB25 migrated to the cell membrane of the AGS cells, and within 24 hours the cancer cells had shrunk in size and lost their ability to adhere to surfaces. In the early stages of exposure, LFcinB25 reduced cell viability through both apoptosis and autophagy (degradation and recycling of obsolete or damaged cell parts). At later stages, apoptosis appeared to dominate, possibly through caspase-dependent mechanisms, and autophagy waned.
“This is the first report describing interplay between apoptosis and autophagy in LFcinB-induced cell death of cancer cells," Chen said.
The research also suggested a target, Beclin-1, which may enhance LFcinB25’s cytotoxic action. Beclin-1 is a protein in humans that plays a central role in autophagy, tumor growth, and degeneration of neurons. In this study, the investigators found that cleaved beclin-1 increased in a time-dependent manner after LFcinB25-exposure, suggesting to the authors a new approach in drug development that may boost the anticancer effects of LFcinB25.
“Gastric cancer is one of the most common causes of cancer-related mortality worldwide, especially in Asian countries," said Wei-Jung Chen, PhD, of the department of biotechnology and animal science of National Ilan University, Taiwan. “In general, the main curative therapies for gastric cancer are surgery and chemotherapy, which are generally only successful if the cancer is diagnosed at an early stage. Novel treatment strategies to improve prognosis are urgently needed."
Researchers evaluated the effects of three peptide fragments derived from lactoferricin B, a peptide in milk that has antimicrobial properties. Only one of the fragments, LFcinB25 reduced the survival of human AGS (Gastric Adenocarcinoma) cells in a dose-dependent and time-dependent manner.
Under a microscope the researchers could see that after one hour of exposure to the gastric cancer cells, LFcinB25 migrated to the cell membrane of the AGS cells, and within 24 hours the cancer cells had shrunk in size and lost their ability to adhere to surfaces. In the early stages of exposure, LFcinB25 reduced cell viability through both apoptosis and autophagy (degradation and recycling of obsolete or damaged cell parts). At later stages, apoptosis appeared to dominate, possibly through caspase-dependent mechanisms, and autophagy waned.
“This is the first report describing interplay between apoptosis and autophagy in LFcinB-induced cell death of cancer cells," Chen said.
The research also suggested a target, Beclin-1, which may enhance LFcinB25’s cytotoxic action. Beclin-1 is a protein in humans that plays a central role in autophagy, tumor growth, and degeneration of neurons. In this study, the investigators found that cleaved beclin-1 increased in a time-dependent manner after LFcinB25-exposure, suggesting to the authors a new approach in drug development that may boost the anticancer effects of LFcinB25.
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