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Archive > Volume 30 Issue 11 > 2023,30(11):973-980. DOI:10.3872/j.issn.1007-385X.2023.11.006 Prev Next
Basic Research
Kanglaite injection regulates cholesterol metabolism to inhibit the malignant biological behavior of lung adenocarcinoma A549 cells
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Abstract:
Objective： To investigate the inhibitory effect of Kanglaite injection (KLTi) on the biological behaviors of lung adenocarcinoma A549 cells by regulating cholesterol metabolism. Methods: An in vitro monoculture model of A549 cells was established. A blank control group (CON group), a KLTi group, a cisplatin group (DDP group) and a KLTi + DDP group were set and given corresponding drug intervention, respectively. CCK-8 method was used to detect the effects of different interventions on the proliferation of A549 cells, and IC50 values were determined for subsequent experiments. The effects of different drugs on the malignant biological behaviors of A549 cells were compared by cell scratch assay, plate clonogenesis assay and Transwell invasion assay, and the late apoptosis of A549 cells were detected by flow cytometry. The expression of epithelial-mesenchymal transition (EMT) related proteins was detected by WB method, and the release level of pro-inflammatory factors was detected by ELISA. Colorimetric method was used to detect the difference of cholesterol content in 106 cells among groups. The difference in the expression levels of membrane channel protein ATP binding cassette transport protein A1 (ABCA1) and functional proteins ATP citrate lyase (ACLY) and peptidylprolyl isomerase B (PPIB) related to cholesterol metabolism was determined by using WB assay. Results: KLTi and DDP inhibited A549 cells in a time- and dose-dependent manner (both P<0.05). Finally, 2 mg/mL KLTi, 3 μg/mL DDP and 48 h of intervention were chosen as intervention dose for follow-up experiments. KLTi alone or combined with DDP could inhibit the clone formation, migration and invasion and promote the late apoptosis of A549 cells, with more prominent effect in the KLTi+DDP group (P<0.05 or P<0.01). KLTi alone or in combination with DDP could improve the EMT process of A549 cells by regulating the proteinexpression of E-cadherin, vimentin and snail (P<0.05 or P<0.01) and down-regulate the release of pro-inflammatory cytokines IL-6 and IL-8 (P<0.05 or P<0.01). KLTi alone or in combination with DDP could significantly reduce the cholesterol content of A549 cells (P<0.05 or P<0.01) and had a regulatory effect on ABCA1, ACLY and PPIB, with more prominent effects in the KLTi+DDP group (P<0.05 or P<0.01). Conclusion: KLTi inhibits the proliferation, migration, invasion and EMT process of lung adenocarcinoma A549 cells possibly by regulating cholesterol metabolism levels and related channel proteins.
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