Mon, Feb 10, 2025 page2

• New cancer signaling mechanism found

  ‘VICIOUS’: The TIMP1-CD63 signaling mechanism, which causes mutated cells to evade destruction, together with DUSP2, which helps those cells grow, triggers cancer growth

  • Staff writer, with CNA
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  Researchers from National Chung Cheng University (CCU) and National Cheng Kung University (NCKU) have identified a novel signaling mechanism in pancreatic cancer patients, knowledge of which might help improve survival rates for the deadly disease.

  The newly-discovered TIMP1-CD63 signaling mechanism causes Kirsten rat sarcoma viral oncogene homologue (KRAS)-mutated cells found in about 90 percent of pancreatic cancer patients to evade destruction by the immune system, the CCU and NCKU said last week.

  The researchers found that a gene deficiency known as dual specificity phosphatase-2 (DUSP2) helps KRAS-mutated cells continue growing.

  

  National Cheng Kung University College of Medicine dean Shan Yan-shen is pictured in an undated photograph.

  Photo: Screen grab from National Cheng Kung University’s Web site

  The interaction of those factors results in a “vicious cycle” that promotes the progression of pancreatic cancer, which has a survival rate of less than 10 percent, the researchers said.

  “Disruption of the vicious cycle ... may be a highly potential way to inhibit pancreatic cancer progression,” the researchers said.

  Led by CCU Department of Physiology chair professor Tsai Shaw-jenq (蔡少正) and NCKU College of Medicine dean Shan Yan-shen (沈延盛), the research team published their findings in the scientific journal Molecular Cancer last month.

  

  National Chung Cheng University Department of Physiology chair professor Tsai Shaw-jenq is pictured in an undated photograph.

  Photo: Screen grab from National Cheng Kung University’s Web site

  The paper, titled “Intercellular TIMP-1-CD63 signaling directs the evolution of immune escape and metastasis in KRAS-mutated pancreatic cancer cells,” was based on in vitro and in vivo experiments on mice, as well as spatial transcriptomic analysis of tumors.

  “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 supports the view that chronic inflammation is a major factor in cancer progression, because it draws a large presence of macrophages — large immune system cells that digest pathogens.

  Based on the interaction of active TIMP-1-CD63 signaling and low DUSP2, the presence of macrophages triggered the “vicious cycle” of tumor growth and might actually play a role in sustaining tumor progression, researchers said.

  The research was primarily funded by Taiwan’s National Science and Technology Council and National Health Research Institutes.
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