by Researchers at the University of California San Diego have made a groundbreaking discovery in which liver cells share molecules through vesicle exchange in order to multiply, even under conditions that would typically suppress cell proliferation. This process, known as vesicle-mediated communication, has also been found to occur in various types of cancer cells, suggesting a potential new target for tackling treatment resistance in cancer.
The study, published in eLife, sheds light on the fundamental issue of cell proliferation and its role in cancer research and biomedical science. The liver was chosen as the focus of the study due to its remarkable regenerative potential. Liver cells have the ability to multiply more rapidly and effectively than any other cells in the body, making them an ideal model for understanding the biological processes that control cell division.
Previous research conducted by the team revealed that a small percentage of liver cells in mice were still able to proliferate, even when genetically modified to lack a critical signaling enzyme called Shp2, which is essential for cell proliferation. Shp2 inhibitors are currently being investigated in clinical trials for their potential in cancer treatment. The researchers discovered that liver cells compensate for the absence of Shp2 by clustering together and exchanging vesicles, which contain the necessary biochemical materials for cell multiplication.
While the initial discovery was made in noncancerous liver cells, further investigation revealed that cancer cells may employ the same strategy to resist treatment and continue dividing. The vesicles used by liver cells to exchange molecules are marked by a protein called CD133, which was found to be abnormally high in various human cancer cells. This suggests that tumors utilize vesicle-mediated communication as a means of evading therapy.
“We believe we’ve discovered an important strategy that tumors use to resist therapy,” said Gen-Sheng Feng, a professor of pathology at UC San Diego School of Medicine. “This discovery could prove to be a powerful new target for cancer treatment, particularly in combination therapies to overcome treatment resistance.”
In addition to offering potential insights into new cancer therapies, the findings challenge conventional thinking about cancer initiation, progression, and recurrence. CD133 is commonly associated with cancer stem cells, which are thought to be responsible for initiating tumors. However, the study suggests that a cancer cell’s “stemness” may not be a permanent characteristic but rather a temporary state that can be induced or even switched off.
“This could be a brand-new way of looking at tumor recurrence that could open doors for new treatments,” said Feng. The discovery of vesicle-mediated communication as a crucial mechanism in cell proliferation and cancer treatment resistance paves the way for innovative approaches in cancer therapy and possible prevention of tumor recurrence.
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