体外研究 (In Vitro) | LCS-1 (1-10000 nM; 24 hours) has selective cytotoxicity towards bloom syndrome gene product (BLM) -proficient and BLM-deficient HCT116 cells[1]. LCS-1 shows growth inhibitory effect on 10/27 adenocarcinoma cell lines (median IC50=0.20 μM; such as H23, H2347, HCC827 cell lines) and normal human bronchial epithelial (NHBE) cells (IC50=2.66 μM)[2]. LCS-1 (0, 1.25, 2 μM; 4 h) in a concentration-dependent manner triggers significant inhibition of SOD1 enzymatic activity in multiple myeloma (MM) cells[3]. LCS-1 (0, 1.25, 2.5, 5 μM; 48 h) in a dose-dependent manner reduces the viability of various MM cell lines, including MM.1R (Dexamethasone-resistant), Dox40 (Doxorubicin-resistant), or LR5 (Melphalan-resistant) cell lines[3]. LCS-1 (48 h) has IC50values of 2.5 and 4.6 μM for cell viability of ANBL6-WT (Bortezomib-sensitive) and ANBL6-BR (Bortezomib- resistant) cells, respectively[3]. LCS-1 (1.25 μM; 16 h) induces a significant increase in ROS levels and O2–levels in MM.1S cells[3]. LCS-1 (1.25 μM; 16 h) shows a significant decrease in GSH/GSSG ratio in MM.1S cells[3]. LCS-1 (1.25 μM; 24h) induces the release of mitochondrial cytochrome-c into the cytosol, and enriches the proteins (HSP60/CLPP) mediating mtUPR signaling in MM.1S cells[3]. LCS-1-induced O2–(1.25 μM; 5 h) triggers a marked decrease in both RP2CP and RP1CP forms of 26S proteasomes[3]. LCS-1 (2 μM; 16 h) induces the early- and late-stage apoptosis of MM.1S cells[3]. LCS-1 (0, 0.5, 1, 1.5, 2 μM) upregulates p53/p21 signaling, as well as downregulates survival pathway proteins MCL-1, BclxL, or c-Myc in MM.1S cells[3]. LCS-1 (0, 4, 8, 16, 24 h; 2 μM) shows a rapid and robust induction of mitochondrial unfolded protein response (UPR) proteins (BIP, PERK, phosphorylated eIF2α, or a lectin protein calnexin) in MM.1S and ANBL6-BR cells[3].
Cell Viability Assay[1] Cell Line: | BLM-proficient and BLM-deficient HCT116 cells | Concentration: | 1-10000 nM | Incubation Time: | 24 hours | Result: | Had IC50values of 1462 nM and 24.92 nM for the viability of BLM-proficient and BLM-deficient HCT116 cells, respectively. |
Western Blot Analysis[3] Cell Line: | MM.1S and ANBL6-BR cells | Concentration: | 2 μM | Incubation Time: | 16 hours | Result: | Decreased the expression of cell-cycle regulatory proteins (cyclin-B1, CDC25C, and CDC2). |
Western Blot Analysis[3] Cell Line: | MM.1S cells | Concentration: | 0, 0.5, 1, 1.5, 2 μM | Incubation Time: | | Result: | Upregulated p53/p21 signaling, as well as downregulated survival pathway proteins MCL-1, BclxL, or c-Myc. |
Western Blot Analysis[3] Cell Line: | MM.1S cells | Concentration: | 2 μM | Incubation Time: | 0, 4, 8, 16, 24 hours | Result: | Showed a rapid and robust induction of UPR proteins (BIP, PERK, phosphorylated eIF2α, or a lectin protein calnexin). |
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