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FEBRUARY 13, 2021 // -- In a recent study published in the international journal EMBO Reports, scientists from the National University of Singapore and others found that a protein called MOAP-1 may play a key role in reducing the risk of liver cancer by inhibiting hyperactive cancer by promoting Nrf2 cell signaling pathfectal pathfectal pathlands.
Photo Source: Chong Teik TAN Hepatocellular Carcinoma (HCC) is the leading form of liver cancer and the fourth leading cause of cancer-related death in the global population, and although researchers have identified a variety of risk factors and genetic variants that induce hepatocellular carcinoma, the prognosis is still poor due to the limited treatment available to patients.
Symptoms of liver cancer-related diseases usually do not appear until the patient's advanced stages of the disease, which further reduces survival;
researcher Victor YU said: 'We found that the MOAP-1 protein reduces levels of insoluble p62 protein aggregates in the liver, which effectively inhibits excessive cell signaling paths called the nuclear factor E2-related factor 2 (Nrf2). Activated; high levels of p62 protein accumulate and form insoluble aggregates in the liver, triggering the overactivation of the Nrf2 signaling path, which in turn enhances the adaptability of cells that open cancer cells and promotes the spread of cancer and evades the immune system.
, there is a strong correlation between high levels of p62 and the occurrence of liver cancer and poor prognosis.
researchers say the MOAP-1 protein is able to physically interact with the p62 protein, interfering with its self-polymerization process, which is thought to play a key role in promoting the insoluble form of p62 aggregation, which causes the p62 protein aggregate to break down, thereby inhibiting its ability to stimulate Nrf2 signaling;
MOAP-1 protein can be regulated by an enzyme-linked mechanism that controls the stability of MOAP-1, and by developing small molecular compounds that manipulate this mechanism, MOAP-1 levels rise in the liver and exert a tumor suppression effect, making it a potential drug candidate for future development of liver cancer therapy.
Researchers are now investigating the key role of moAP-1 protein in the development of non-alcoholic fatty liver disease (NAFLD), the leading cause of hepatocellular carcinoma in the global population (and even singapore).
Final researcher Yu said NAFLD includes a range of liver diseases, from fatty degeneration to non-alcoholic fatty liver disease, as well as development into life-threatening liver diseases, including cirrhosis and hepatocellular carcinoma;
this study, they found that the MOAP-1 protein may act as a regulator of the p62 protein, and later researchers will continue to explore the key role of the MOAP-1 protein in the development of NAFLD and hepatocellular carcinoma.
() Original source: Chong Teik Tan, Hao-Chun Chang, Qiling Zhou, et al. MOAP‐1‐mediated dissociation of p62/SQSTM1 bodies releases Keap1 and suppresses Nrf2 signaling, EMBO reports (2021). DOI:10.15252/embr.20205085