human lung derived a549 cells  (InvivoGen)

Journal: mBio

Article Title: Novel Klebsiella pneumoniae and Pseudomonas aeruginosa MAPS vaccine combining O polysaccharides and pathogen-specific proteins

doi: 10.1128/mbio.00807-25

Figure Lengend Snippet: Functional activity of preimmune and immune sera generated in rabbits by pathogen-relevant fusion proteins in 12-valent KPPA MAPS vaccine. ( A ) MrkA antibody function. Cells: A549 lung epithelial-derived tissue culture; bacteria: Klebsiella strain 1015 O4:K15 (not in vaccine). ( B ) PcrV antibody function . Pseudomonas injection of cytotoxins through T3SS induces apoptosis of lung epithelial cells, as indicated by loss of Alamar Blue dye absorbance. Cells: A549 lung-epithelial-derived tissue culture; bacteria: Pseudomonas strain PAK (known to express PcrV and cytotoxins). ( C ) FlaB antibody function. Soft agar motility inhibition assay. Bacteria: Pseudomonas FlaB+ strain PAO1 was added in quadruplicate to soft agar containing either preimmune or KPPA MAPS post-immune sera, and ( D ) the diameter of PA migration from the central stab was measured.

Article Snippet: Human lung epithelium-derived A549 cells (ATCC CRM-CCL-185) were grown at 37°C and 5% CO 2 in F-12K nutrient medium with L-glutamine supplemented with 10% FBS and penicillin/streptomycin antibiotic.

Techniques: Functional Assay, Activity Assay, Generated, Derivative Assay, Bacteria, Injection, Inhibition, Migration

Journal: mBio

Article Title: Novel Klebsiella pneumoniae and Pseudomonas aeruginosa MAPS vaccine combining O polysaccharides and pathogen-specific proteins

doi: 10.1128/mbio.00807-25

Figure Lengend Snippet: MAPS-elicited antisera inhibit adherence of MrkA+ KP to A549 lung epithelial cells but not of MrkA− KP. ( A ) Rabbits were immunized with NCB014 or with Rhavi FlaB D2-MrkA-his alone on a K19 backbone, and the sera were tested for the ability to inhibit the adherence of a MrkA+ (KP1015) or a MrkA− KP strain (strain 11818/3) to A549 cells. The MrkA-immune sera (NCB014), but not the preimmune (P0), reduced the adherence of the MrkA+, but not that of the MrkA− KP strain, similar to the inhibition with the MrkA-only antisera. ( B ) Neither NCB014 immune nor MrkA-specific antisera were able to inhibit the binding of a MrkA− KP strain.

Article Snippet: Human lung epithelium-derived A549 cells (ATCC CRM-CCL-185) were grown at 37°C and 5% CO 2 in F-12K nutrient medium with L-glutamine supplemented with 10% FBS and penicillin/streptomycin antibiotic.

Techniques: Inhibition, Binding Assay

Journal: ACS Omega

Article Title: Novel C-2 Aromatic Heterocycle-Substituted Triterpenoids Inhibit Hedgehog Signaling in GLI1 Overexpression Cancer Cells

doi: 10.1021/acsomega.4c11479

Figure Lengend Snippet: Effect of compounds 11a and 11b on the protein expression of the Gli1 transcription factor and its transcriptional targets in A549 (A) and DU145 (B) cells following 24 h of incubation. An antibody against GAPDH was used as an internal loading control.

Article Snippet: The human lung tumor-derived cell line A549 was obtained from ATCC and cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) supplemented with 10% FBS.

Techniques: Expressing, Incubation, 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: 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