human non small cell lung cancer nsclc cell lines a549  (ATCC)

Journal: Drug Design, Development and Therapy

Article Title: Rhein Alleviates Cisplatin-Induced Acute Kidney Injury via Downregulation of NOX4-COX2/PGFS Signaling Pathway

doi: 10.2147/DDDT.S515409

Figure Lengend Snippet: Rhein reduces CDDP-induced nephrotoxicity without affecting the antitumor efficacy. CDDP (10μg/mL)-treated human non-small-cell lung cancer (NSCLC) A549 cells were incubated with 40 μM Rhein for 24 h. ( A ) The cell viability was determined by the CCK8 analysis (n=6). ( B ) The CDDP-sensitive Lewis lung carcinoma (LLC) cells (2×10 5 ) were inoculated subcutaneously into C57BL/6 mice for 14 days, and the mice were treated with CDDP alone (4 mg/kg, the drugs were administered every other day for 10 days, resulting in an accumulative dose of 20 mg/kg) or combination with Rhein (80mg/kg, the drugs were administered 1 hour after CDDP injection). ( C and D ) The xenograft tumor weights and tumor volume of C57BL/6 mice injected subcutaneously with LLC cells with the treatment of CDDP, Rhein alone or in combination with Rhein (n=5). Data are shown as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001: CDDP vs Control. ## P < 0.01 CDDP+Rhein vs CDDP.

Article Snippet: To determine whether Rhein might affect the anti-tumor activity of CDDP in vitro, CDDP-sensitive human non-small-cell lung cancer (NSCLC) cell line A549 (catalog no. CCL-185, RRID: CVCL_0023; ATCC, Manassas, VA, USA) was exposed to CDDP (10 μg/mL) alone or in combination with Rhein for 24h, cell viability was then measured.

Techniques: Incubation, Injection, Control

Journal: bioRxiv

Article Title: Comparative study of the mechanism of natural compounds with similar structures using docking and transcriptome data for improving in silico herbal medicine experimentations

doi: 10.1101/2023.04.23.538005

Figure Lengend Snippet: The A549 cell line was treated with oleanolic acid (OA), hederagenin (HG), a combination of OA and HG (COH), and gallic acid (GA), and the mechanism of action of each compound was derived using transcriptome data. Gene set enrichment analysis (GSEA) was performed using the gene expression results derived from each compound. (A) Venn diagram is shown using the genes selected as DEGs as a result of RNA-seq analysis of OA, HG, COH, and GA. Commonly selected DEGs in OA, HG, and COH are highlighted in orange circles. (B) A volcano plot was constructed using gene expression information derived from COH. (C) GSEA results of OA, HG, COH and GA were calculated using the KEGG pathway gene sets and RNA-seq analysis results of OA, HG, COH and GA.

Article Snippet: Human non-small cell lung cancer cells (NSCLC) line A549 (CCL-185) was purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Derivative Assay, Gene Expression, RNA Sequencing, Construct

Journal: Oncology Research

Article Title: Cisplatin-induced activation of TGF-β signaling contributes to drug resistance

doi: 10.32604/or.2023.030190

Figure Lengend Snippet: Effect of cisplatin on various types of cancer cell lines. (A) Cisplatin enhanced N-cadherin expression in A549 but not in DLD-1, HCT116, HT29, SW48, and LNCaP cells. Cells were treated with 1 μM cisplatin for the indicated periods (0, 3, 6, 9, and 12 days). The protein expression of N-cadherin and β-actin was detected by western blotting. Images are representative of two independent experiments. (B) Cisplatin decreased E-cadherin mRNA, and increased N-cadherin and Slug mRNAs in A549 cells. A549 cells were treated with 1 μM cisplatin for the indicated periods. The amount of E-cadherin, N-cadherin, and Slug mRNAs were evaluated using qPCR. The presented data are normalized to Day 0. All data are representative of three independent experiments and presented as mean SD ± (n = 3). * p < 0.05 and ** p < 0.01 (two-tailed Student’s test). (C) The TβRI kinase inhibitor, SB431452, partially suppressed cisplatin-induced Slug upregulation in A549 cells. A549 cells were treated with 10 μM cisplatin and/or 1 μM SB431452. Twenty-four hours later, the cells were collected and subjected to qPCR analysis to detect Slug mRNA. The presented data are normalized to control cells. All data are representative of three independent experiments and presented as mean SD ± (n = 3). * p < 0.05 and ** p < 0.01 (two-tailed Student’s test). (D) TGF-β1 induces and decreases N-cadherin and E-cadherin in LoVo and A549 cells. Cells were stimulated with the indicated concentrations of TGF-β1 (0, 0.1, 1, 10 ng/mL). Two days later, the cells were collected and subjected to western blot analysis to detect E-cadherin, N-cadherin, and β-actin.

Article Snippet: Human colorectal adenocarcinoma-derived cell line HCT116, HT29, and DLD-1, human non-small cell lung cancer (NSCLC) adenocarcinoma-derived cell line A549, and human prostate cancer-derived cell line LNCaP were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Expressing, Western Blot, Two Tailed Test, Control

Journal: Oncology Research

Article Title: Cisplatin-induced activation of TGF-β signaling contributes to drug resistance

doi: 10.32604/or.2023.030190

Figure Lengend Snippet: Cisplatin enhances the secretion of TGF-β1. (A) Cisplatin increased the amount of TGF-β1 in the culture media from LoVo and A549 cells. LoVo and A549 cells were treated with 1 μM cisplatin for 72 h. The culture media from cells were collected and subjected to ELISA to measure the amount of TGF-β1. The amounts of TGF-β1 from LoVo and A549 cells without cisplatin were used to calculate relative values. All data are presented as mean SD ± (n = 3). *** p < 0.001 (two-tailed Student’s test). (B) The amount of TGF-β1 in the culture media from cisplatin r /LoVo cells were increased. The culture media from LoVo or cisplatin r /LoVo (#10, #19, and #54) cells were collected and subjected to ELISA to measure the amount of TGF-β1. The amount of TGF-β1 from LoVo cells without cisplatin was used to calculate relative values. All data are presented as mean SD ± (n = 3). ** p < 0.01 and *** p < 0.001 (two-tailed Student’s test). (C) The effect of cisplatin on the expression of TGF-β1 mRNA in LoVo cells. LoVo cells were treated with 1 μM cisplatin. Three days later, the total RNA was extracted and subjected to qPCR analysis to measure the amount of TGF-β1 mRNA. The presented data are normalized to control cells. All data are representative of three independent experiments. (D) The comparison of the expression levels of TGF-β1 mRNA in LoVo and cisplatin r /LoVo cells. Total RNA from exponentially growing LoVo or cisplatin r /LoVo cells (#10, #19, and #54) was extracted and subjected to qPCR analysis to measure the amount of TGF-β1 mRNA. The presented data are normalized to LoVo cells. All data are representative of three independent experiments.

Article Snippet: Human colorectal adenocarcinoma-derived cell line HCT116, HT29, and DLD-1, human non-small cell lung cancer (NSCLC) adenocarcinoma-derived cell line A549, and human prostate cancer-derived cell line LNCaP were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Enzyme-linked Immunosorbent Assay, Two Tailed Test, Expressing, Control, Comparison