Researchers from National Chung Cheng University (CCU) and National Cheng Kung University (NCKU) have uncovered a previously unknown signalling mechanism that allows pancreatic cancer cells to evade immune defenses and sustain tumor growth, as reported by the Taipei Times.
Their findings could pave the way for new treatment strategies for one of the deadliest cancers, which has a survival rate of less than 10%.
Key Findings
The study, published in the journal Molecular Cancer, highlights the role of the TIMP1-CD63 signalling mechanism in protecting KRAS-mutated pancreatic cancer cells from immune system attacks. These mutations are found in approximately 90% of pancreatic cancer patients.
Additionally, a deficiency in the dual-specificity phosphatase-2 (DUSP2) gene allows these cancerous cells to grow uncontrollably, creating a self-sustaining cycle that accelerates tumor progression.
“Disruption of the vicious cycle … maybe a highly potential way to inhibit pancreatic cancer progression,” researchers in Taiwan stated.
Study Insights
The research was led by Professor Tsai Shaw-jenq from CCU’s Department of Physiology and Dean Shan Yan-shen from NCKU’s College of Medicine. Their study was conducted using laboratory experiments on mice and spatial transcriptomic analysis of tumor samples.
Shan emphasized:
“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.”
The study also reinforces the link between chronic inflammation and cancer progression. Researchers found that macrophages, immune cells typically responsible for eliminating harmful pathogens, actually contribute to tumor growth under specific conditions.
Furthermore, the interaction between active TIMP1-CD63 signalling and low DUSP2 levels was observed to increase macrophage presence, fueling the self-perpetuating cycle of cancer development.
Funding & Future Research
The study was funded by Taiwan’s National Science and Technology Council and the National Health Research Institutes. Researchers hope their discovery will lead to new therapeutic strategies aimed at disrupting the TIMP1-CD63 pathway to slow down or halt pancreatic cancer progression.
This breakthrough provides a promising avenue for future cancer treatments and highlights the importance of immune system interactions in tumor development.