Previous evidence showed ${eta}1$, 3-N-acetylglucosaminyltransferase 8 (${eta}3GnT8$), which can extend polylactosamine on N-glycans, to be highly expressed in some cancer cell lines and tissues, indicating roles in tumorigenesis. However, so far, the function of ${eta}3GnT8$ in laryngeal carcinoma has not been characterized. To test any contribution, Hep-2 cells were stably transfected with sense or interference vectors to establish cell lines that overexpressed or were deficient in ${eta}3GnT8$. Here we showed that cell proliferation was increased in ${eta}3GnT8$ overexpressed cells but decreased in ${eta}3GnT8$ knockdown cells using MTT. Furthermore, we demonstrated that change in ${eta}3GnT8$ expression had significant effects on tumor growth in nude mice.We further provided data suggesting that overexpression of ${eta}3GnT8$ enhanced the expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) at both the mRNA and protein levels, associated with shedding of tissue inhibitors of metalloproteinase TIMP-2. In addition, it caused increased production of transforming growth factor beta 1 (TGF-${eta}1$), whereas ${eta}3GnT8$ gene knockdown caused the reverse effect. The results may indicate a novel mechanism by which effects of ${eta}3GnT8$ in regulating cellular proliferation are mediated, at least in partvia targeting MMPs/TIMPs and TGF-${eta}1$ in laryngeal carcinoma Hep-2 cells. The finding may lay a foundation for further investigations into the ${eta}3GnT8$ as a potential target for therapy of laryngeal carcinoma.