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The semiconducting ferromagnet CrSiTe3 is a promising candidate for two-dimensional magnet simply by exfoliating down to single layers. To understand the magnetic behavior in thin-film samples and the possible applications, it is necessary to establish the nature of the magnetism in the bulk. In this work, the critical behavior at the paramagnetic to ferromagnetic phase transition in single-crystalline CrSiTe3 is investigated by bulk magnetization measurements. We have obtained the critical exponents (β = 0.170 ± 0.008, γ = 1.532 ± 0.001, and δ = 9.917 ± 0.008) and the critical temperature TC = 31.0 K using various techniques such as modified Arrott plot, Kouvel-Fisher plot, and critical isotherm analysis. Our analysis suggests that the determined exponents match well with those calculated from the results of renormalization group approach for a two-dimensional Ising model coupled with long-range interaction.

Chemotherapy and radiation not only trigger cancer cell apoptosis but also damage stromal cells in the tumour microenvironment (TME), inducing a senescence-associated secretory phenotype (SASP) characterized by chronic secretion of diverse soluble factors. Here we report serine protease inhibitor Kazal type I (SPINK1), a SASP factor produced in human stromal cells after genotoxic treatment. DNA damage causes SPINK1 expression by engaging NF-κB and C/EBP, while paracrine SPINK1 promotes cancer cell aggressiveness particularly chemoresistance. Strikingly, SPINK1 reprograms the expression profile of cancer cells, causing prominent epithelial-endothelial transition (EET), a phenotypic switch mediated by EGFR signaling but hitherto rarely reported for a SASP factor. In vivo, SPINK1 is expressed in the stroma of solid tumours and is routinely detectable in peripheral blood of cancer patients after chemotherapy. Our study substantiates SPINK1 as both a targetable SASP factor and a novel noninvasive biomarker of therapeutically damaged TME for disease control and clinical surveillance.