On the reactivity of complexes [Ni(NHC)] with CS.

A study of the reaction of [Ni(NHC)] synthons with the heterocumulene CS is reported. Nickel complexes of η-(C-S) coordinated CS, [Ni(NHC)(η-CS)] (NHC = IiPr (1a), IiPr (1b)) were obtained from the reaction of CS with precursors of [Ni(NHC)] (NHC = IiPr, IiPr). The result of this reaction critically depends on the NHC employed, as [Ni(IMes)], the complex of the sterically more demanding -aryl substituted NHC IMes, led to formation of the dinuclear complex [{Ni(IMes)(μ-CS)}] (2d).

SMYD3 drives cell cycle and epithelial-mesenchymal transition pathways through dual gene transcriptional repression and activation in HPV-negative head and neck cancer.

Human papillomavirus (HPV)-negative head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer type in the world and is associated with an overall poor prognosis. The protein methyltransferase SET and MYND domain-containing 3 (SMYD3), which trimethylates H3K4, activates gene transcription and enhances several oncogenic pathways, including epithelial-mesenchymal transition and cell cycle related pathways, in various cancer types. It was also recently shown that SMYD3 is overexpressed in HPV-negative HNSCC, and represses the expression of type I IFN response genes, contributing to resistance to anti-PD-1 checkpoint blockade in this disease.

Radical anions of 1,1-azoliumdithiocarboxylates.

The 1,1-azoliumdithiocarboxylate cAAC-CS (1a) was prepared and its redox chemistry was evaluated and compared to NHC based dithiocarboxylates IDipp-CS (1b) and IMes-CS (1c). Radical anions [carbene-CS]˙ were prepared by metallic reduction as the potassium or magnesium ion complexes [K(18-crown-6)(cAAC-CS)] (2a), [K(18-crown-6)(NHC-CS)] (NHC = IDipp: 2b, IMes: 2c), and [Mg(NacNac)(cAAC-CS)] (3) and extensively characterized (SC-XRD, EPR, UV/VIS/NIR, DFT). These complexes represent the first examples of isolated radical anions of 1,1-dithiolenes.

Smyd3-mediated immuno-modulation in HPV-negative head and neck squamous cell carcinoma mouse models.

SET and MYND-domain containing protein 3 (SMYD3) mediates epigenetic repression of type I IFN response genes in human papillomavirus (HPV)-negative HNSCC cells, and Smyd3 depletion using anti-sense oligonucleotides (ASOs) increases the sensitivity of syngeneic mouse oral carcinoma (MOC1) models to anti-PD-1 therapy. In this study, we utilized single-cell RNA-seq of MOC1 tumors treated with Smyd3 ASOs and found enrichment of type I IFN response pathways in cancer cells, a shift of CD8 T-cells toward an activated/memory phenotype, and a shift of neutrophils toward an anti-tumorigenic phenotype. Mechanisms of resistance to the Smyd3 ASO and anti-PD-1 combination were derived from cancer cells, macrophages, and CD8 T-cells, including neutrophil enrichment through the upregulation of , repression of and defective antigen presentation.

The tetracyanoborate anion as a building block for the heterocubane cluster cage [Cr{B(CN)}].

The tetracyanoborate anion [B(CN)] (TCB) was utilized as a building block for the synthesis of polynuclear chromium carbonyl compounds upon photolytic reaction with [Cr(CO)]. Up to four κN-coordinated cyano groups of TCB can be involved in binding to chromium, giving mixtures of [B(CN){CN-Cr(CO)}] ( = 1-4; 1-4) and [{Cr(CO)(B(CN))}] (5). The reaction of [B(CN)] with -[Cr(CO)(MeCN)] led to isolation of salts of the tetraanionic heterocubane cage [{Cr(CO)(B(CN))}].