Dgkz, also known as Diacylglycerol kinase ζ, is a diacylglycerol kinase that metabolizes diacylglycerol to yield phosphatidic acid. It is involved in lipid signaling pathways which are crucial for neural activities, memory, and learning [3]. It has been associated with various biological processes and diseases, with its role being explored through different genetic models.

In triple-negative breast cancer, knockout of Dgkz in cell lines significantly inhibited metastatic behaviors in vitro and in vivo, indicating its role as a prometastatic gene by promoting the TGFβ signaling pathway through suppressing lipid raft-dependent endocytosis of TGFβR2 [1]. In osteosarcoma, silence of Dgkz by shRNA hampered cell growth and promoted apoptosis in vitro, and its knockout suppressed xenograft tumor proliferation in vivo, suggesting it acts as an oncogene potentially interacting with the ERK1/2 and MYC pathway [2]. Similar tumor-suppressing effects of Dgkz knockdown were seen in cervical cancer and acute myeloid leukemia, with impacts on cell proliferation, apoptosis, and cell cycle arrest [4,5].

In conclusion, Dgkz plays significant roles in cancer progression, including in triple-negative breast cancer, osteosarcoma, cervical cancer, and acute myeloid leukemia. Knockout and knockdown studies in cell lines and in vivo models have revealed its oncogenic potential in promoting tumor cell growth, metastasis, and survival, highlighting its importance as a potential therapeutic target in these cancer types.