- Taiwanese scientists discovered that the TIMP1-CD63 pathway helps KRAS-mutated pancreatic cancer cells evade immune attacks and sustain growth.
- A deficiency in the DUSP2 gene allows unchecked tumor progression, reinforcing a self-sustaining cycle that accelerates pancreatic cancer development.
Scientists in Taiwan have identified a signaling mechanism that helps pancreatic cancer cells evade immune defenses. The research, conducted by National Chung Cheng University (CCU) and National Cheng Kung University (NCKU), was reported by the Taipei Times.
The study identifies the TIMP1-CD63 signaling pathway as a key factor in protecting KRAS-mutated pancreatic cancer cells, which are found in nearly 90% of cases, from immune system attacks.
Researchers also found that a deficiency in the gene DUSP2 allows these cancer cells to multiply unchecked. Together, these factors create a cycle that speeds up tumor growth.
With pancreatic cancer’s survival rate below 10%, the findings highlight a potential way to slow the disease.
“Disruption of the vicious cycle ... may be a highly potential way to inhibit pancreatic cancer progression,” the researchers stated.
The study was led by CCU Department of Physiology Chair Professor Tsai Shaw-jenq and NCKU College of Medicine Dean Shan Yan-shen. It was published last month in Molecular Cancer and involved laboratory experiments on mice and spatial transcriptomic analysis of tumor samples.
“Understanding interactions between various cells in pancreatic cancer tumor micro-environments is of great significance for developing blocking strategies, improving early diagnosis rates and improving patient prognoses,” Shan said.
The research also found that macrophages, immune cells that usually destroy harmful pathogens, may instead contribute to tumor growth under the influence of TIMP1-CD63 signaling and low DUSP2 levels.
The study was funded by Taiwan’s National Science and Technology Council and the National Health Research Institutes.
Edited by Harshajit Sarmah
