## 4 Discussion  
In this study, we characterized the SI powder fabric and its radiation of 37.2 mW/cm\({}^{2}\). The radiation power density was slightly higher than other FIR-emitting fabrics [1]. This fabric showed cell viability inhibiting properties. The decreases in cell viability resulted from reduced ATP production (Figure 2). Initial ATP level indicates the physiological state of the cell [28], and ATP depletion is a proxy for cell proliferation inhibition [29]. In addition, a reduced basal intracellular ATP concentration correlates with cell viability [30]. Thus, exposure to FIR triggers ATP depletion, forcing cancer cells into halting cell proliferation [15]. To induce such ATP depletion in cells through cell pathways, we performed transcriptional microarray analyses. The results showed 1231 upregulated and 1200 downregulated genes, with fold changes exceeding 1.5 (\(p<0.05\)). Among upregulated genes, apoptosis-related genes were classified as membrane attack complex, natural killer cell-mediated cytotoxicity, and zinc finger-related genes. These genes also appeared in the gene enrichment and KEGG pathways. The GO enrichment analysis of pathways regulated by these genes showed that SI-exposure activated transmembrane signaling receptor genes and G protein-coupled receptor genes. The transmembrane signaling receptor transduced an extracellular signal across the cell membrane, initiating a change in cell physiology. The G protein-coupled receptor sensed a chemoattractant and activated a membrane-associated G protein, promoting the exchange of GDP for GTP on the alpha subunit of the heterotrimic G protein complex. According to GO annotations, the transmembrane signaling receptor activity involves a number of G protein-coupled receptors. Such gene enrichments correspond to pathway enrichments in KEGG analysis (Figure 3). According to the KEGG analysis, systemic lupus erythematosus is particularly related to the MAC pathways. MAC is a cytolytic effector of innate and adaptive immunity that forms pores in the plasma membrane of pathogens or targeted cells, leading to osmolysis [26]. Osmolysis disrupts the cell membrane of target cells, leading to cell death [31] because the MAC, composed of the complement components C5b, C6, C7, C8, and several C9 molecules [26], needs to be assembled first. To assemble MAC, C5 leaves into the small anaphylatoxin C5a and the large fragment C5b by C5 convertase. C6 binds the labile C5b intermediate, resulting in a stable C5b6 complex. C7 binds C5b-6, anchoring the newly formed C5b-7 complex to the membrane surface. C8 (composed of C8\(\alpha\), C8\(\beta\), and C8\(\gamma\)) is incorporated into the assembly precursor to form the C5b-8 initiator complex, marking the  
Figure 5: Changes in protein expression of C7 and C8b after FIR exposure: (**A**) changes in protein expression; (**B**) western blotting analysis. Data are shown as the mean \(\pm\) standard deviation (\(n=3\)) after a two-tailed paired Student’s \(t\)-test (**_p_\(<0.01\)). first membrane permeation event. Finally, multiple copies of C9 join the assembly and cross the membrane, ultimately creating the final MAC [26; 32]. The pore formation facilitates the entry of toxic substances into the cell, such as nitrogen oxide and oxygen radicals, which further stimulate cells to produce inflammatory mediators and growth factors, leading to cell proliferation inhibition [33; 34]. [PERSON] et al. reported the C5b-9-mediated inhibition of endothelial cell proliferation [35]. [PERSON] et al. reported that C5b-9 inhibited cell proliferation in rat mesangial cells through caspase activation [27; 36]. In this study, C5, C6, C7, and C8\(\emptyset\) were significantly expressed, as evidenced by qPCR. These activations imply that FIR exposure triggered C5 to form MACs in cancer cells. According to this mechanism, C8, as a heterotrimic complex, undergoes a conformational rearrangement, with the C8\(\alpha\) subunit being the first component to penetrate the lipid bilayer [37].