Crack the code of cancer king’s transformation! Scientists inhibit 1 gene to reverse malignant pancreatic cancer cells

Schematic diagram of the location and structure of the human pancreas. Because early symptoms are not obvious, pancreatic cancer has long been regarded as one of the cancers with the highest mortality rate and the most difficult to treat.

[Compiled by Chen Chengliang/Comprehensive Report] Pancreatic cancer is difficult to treat. One of the reasons is that the cancer cells in the tumor are not all the same. Some grow more aggressively while others grow more slowly. An American research team discovered that a gene called MYC may be an important factor in maintaining the high malignancy of some pancreatic cancer cells. In cell experiments, after inhibiting MYC activity, some more aggressive cancer cells transformed into another less aggressive form.

The technology media "SciTechDaily" reported that this study, conducted by a research team at NYU Langone Health, was published in "Nature Genetics". The team analyzed tumor samples from 56 patients and examined more than 440,000 cells to understand the characteristics of different cancer cells within the same tumor.

The research team classified pancreatic cancer cells into "basal type" and "classic type". The basal type is usually more aggressive, while the classic type is less aggressive. Both types may coexist in the same tumor, indicating that the cancer cells are not identical.

The researchers found that the MYC gene is particularly active in more aggressive cancer cells. In cell experiments, after inhibiting MYC activity, some basal cancer cells transformed into classic cancer cells. This result shows that MYC may be involved in maintaining the malignant characteristics of cancer cells, and also gives researchers the opportunity to further explore whether they can change the behavior of cancer cells by intervening in related mechanisms.

Research has also found immune-related clues, and the therapeutic effect still needs to be verified

In addition to MYC, the research team also observed the TIGIT protein related to immune regulation. The discovery provides another avenue for research into understanding the interaction between pancreatic cancer cells and the body's immune system, and how some cancer cells evade immune attack.

The MYC and TIGIT-related mechanisms involved in the study may provide clues for future treatment strategies, but changes in cell morphology do not mean tumor shrinkage, nor does it mean that the patient's condition will improve as a result. The results of this study still need to be confirmed through follow-up studies to determine whether the relevant findings can be developed into effective treatments for pancreatic cancer.