was also found that the HCC patients who have a relatively lower histological grade inversely possess a higher level of expression in EMP3. Then, the researchers found that knockdown (gene silencing) of EMP3 resulted in reduction of cell proliferation and arrest of cell cycle, which suggests a potential role of EMP3 in tumor-suppressing. Brain cancer EMP3 is found to play a large role in the progression of neuroblastomas and glioblastomas, which are two of the most common types of brain cancers. Both have fast carcinogenesis result in a high rate of mortality. EMP3 is proposed as an oncogene whose overexpression in the progression correlated with glioblastoma (GBM). Reduction in EMP3 expression in CD44-high GBM cell lines promotes apoptosis of the cancer cell lines and disables potential tumorigenesis. One of the signaling activation pathway involving EMP3 in the progression of glioblastoma was identified in 2016. The pathway was identified as TGF-β/Smad2/3 signaling, in which the unregulated TGF-β signaling promotes tumorigenesis in various human cells, especially CD44-high glioma cells. The interaction between EMP3 and the receptor of TGF-β regulate the TGF-β/Smad2/3 signaling activation, which eventually suppresses cell proliferation and weakens tumorigenesis in glioblastoma. Clinical significance Due to the controversial effects of EMP3 on tumor suppression, the applicable treatments for certain carcinomas related to EMP3 are still unvalidated in humans. However, some animal experiments have showed a positive result on suppressing the tumorous tissues by modifying the EMP3 gene. References