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Researchers from National Chung Cheng University (CCU) and National Cheng Kung University (NCKU) have identified a previously unknown signaling mechanism that enables pancreatic cancer cells to evade immune defenses and sustain tumor growth, as reported by the Taipei Times.
Their findings could contribute to the development of new treatment approaches for one of the deadliest forms of cancer, the report added. According to the Taipei Times, the study reveals that the TIMP1-CD63 signalling mechanism plays a critical role in protecting Kirsten rat sarcoma viral oncogene homologue (KRAS)-mutated pancreatic cancer cells--found in approximately 90 per cent of patients--from being destroyed by the immune system. In addition, a deficiency in the gene known as dual-specificity phosphatase-2 (DUSP2) allows these mutated cells to continue growing unchecked. Together, these mechanisms create a self-sustaining cycle that accelerates cancer progression, the report said. With pancreatic cancer's survival rate at less than 10 per cent, researchers emphasised the significance of this discovery. "Disruption of the vicious cycle ... maybe a highly potential way to inhibit pancreatic cancer progression," researchers in Taiwan said.. The research, led by CCU Department of Physiology Chair Professor Tsai Shaw-jenq and NCKU College of Medicine Dean Shan Yan-shen, was published last month in the journal Molecular Cancer, as reported by the Taipei Times. Their study, titled Intercellular TIMP-1-CD63 signalling directs the evolution of immune escape and metastasis in KRAS-mutated pancreatic cancer cells, was based on laboratory experiments using mice, along with spatial transcriptomic analysis of tumour samples. "Understanding interactions between various cells in pancreatic cancer tumour micro-environments is of great significance for developing blocking strategies, improving early diagnosis rates and improving patient prognoses," Shan said. The research also reinforces the link between chronic inflammation and cancer progression, as immune cells known as macrophages--normally responsible for digesting harmful pathogens--appear to contribute to tumor growth under specific conditions, the report added. Further, as per the Taipei Times, researchers observed that the interaction between active TIMP1-CD63 signaling and low DUSP2 levels led to an increased macrophage presence, which in turn fueled the self-perpetuating cycle of tumor development. The study was primarily funded by Taiwan's National Science and Technology Council and National Health Research Institutes. (ANI)
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