The carbon-coated Ni(C) nanocapsules were prepared by a modified arc-discharge method in methane atmosphere. Its electromagnetic parameters were measured at $2–18\mathrm{GHz}$ . It is observed that the natural resonance which appeared at $5.5\mathrm{GHz}$ is dominant among microwave absorption properties of Ni(C) nanocapsules, as the consequence of the increased surface anisotropic energy for nanosized particles. The measured relative complex permittivity indicates that a high resistivity existed in Ni(C) nanocapsules samples. The maximum reflection loss of Ni(C) nanocomposites can reach $32\mathrm{dB}$ at $13\mathrm{GHz}$ with $2\mathrm{mm}$ in thickness. The microwave absorptive mechanisms of Ni(C) nanocapsule absorbent were discussed.

Glutaminase (GLS), which converts glutamine to glutamate, plays a key role in cancer cell metabolism, growth, and proliferation. GLS is being explored as a cancer therapeutic target, but whether GLS inhibitors affect cancer cell–autonomous growth or the host microenvironment or have off-target effects is unknown. Here, we report that loss of one copy of Gls blunted tumor progression in an immune-competent MYC-mediated mouse model of hepatocellular carcinoma. Compared with results in untreated animals with MYC-induced hepatocellular carcinoma, administration of the GLS-specific inhibitor bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide (BPTES) prolonged survival without any apparent toxicities. BPTES also inhibited growth of a MYC-dependent human B cell lymphoma cell line (P493) by blocking DNA replication, leading to cell death and fragmentation. In mice harboring P493 tumor xenografts, BPTES treatment inhibited tumor cell growth; however, P493 xenografts expressing a BPTES-resistant GLS mutant (GLS-K325A) or overexpressing GLS were not affected by BPTES treatment. Moreover, a customized Vivo-Morpholino that targets human GLS mRNA markedly inhibited P493 xenograft growth without affecting mouse Gls expression. Conversely, a Vivo-Morpholino directed at mouse Gls had no antitumor activity in vivo. Collectively, our studies demonstrate that GLS is required for tumorigenesis and support small molecule and genetic inhibition of GLS as potential approaches for targeting the tumor cell–autonomous dependence on GLS for cancer therapy.