Advanced searches left 3/3

A549 Cell - Europe PMC

Summarized by Plex Scholar
Last Updated: 10 June 2022

* If you want to update the article please login/register

Acute cytotoxicity, genotoxicity, and apoptosis induced by petroleum VOC emissions in A549 cell line.

Petroleum fugitive VOC inhalation by petrol station attendants has been widely linked to toxicological and health risks. Using A549 cells, the study investigated the cytotoxic and genotoxic end points resulting from whole gasoline fumes in vitro exposure. VOCs were first identified and characterized by GC-MS. The VOCs were mimicted in a controlled environment by evaporating high-carbons in a closed exposure chamber in a controlled environment. The findings revealed that acute gasoline whole VOCs exposure impaired cell viability, undermined cell membrane integrity, caused cell membrane integrity, and caused DNA damage. Overall, the static exposure method's results showed a robust and reproducible model that can be used to evaluate acute crude VOC mixture toxicity endpoints and cell death pathways.

Source link: https://europepmc.org/article/MED/35675845


8-HOQ a natural chelating agent from Streptomyces spp inhibits A549 lung cancer cell lines via BCL2/STAT3 regulating pathways

"The finding of biochemical chemotherapeutic compounds from soil Streptomyces spp. " For A549 lung cancer cell lines, a cytotoxicity test revealed that 8-HOQ had potent anticancer effects with IC 50 values of 26 h, 48 h, and 72 h respectively against A549 lung cancer cell lines. The results also showed that 8-HOQ from Streptomyces spp significantly reduced the A549 lung cancer cell lines and stimulated apoptosis' intrinsic pathways. The caspase-3 and 8 activities could have been enhanced in 8-HOQ-treated A549 cell lines, and the WHOQ reported that 8-HOQ mediated A549 cancer cell death by the intrinsic pathway. In A549 cell lines, expression of P53, BCL2, and STAT3 was blocked, indicating the metastasis inhibitory potential of 8-HOQ by blocking migration and invasion in A549 cell lines. Cell lines from A549 lung cancer cells lines can potentially hindered expansion and migration.

Source link: https://europepmc.org/article/PPR/PPR501529


Effect of the elastin-derived peptides (VGVAPG and VVGPGA) on breast (MCF-7) and lung (A549) cancer cell lines in vitro.

"Elastin, one of the ECM's key components, is the aging process, and releases elastin-derived peptides. " Because of this, the current study was conducted to determine the effect of VGVAPG hexapeptide and elastin-like peptide VVGPGA on certain physiological characteristics in human breast adenocarcinoma and human lung carcinoma cell lines. Following 24-h therapy, VGVAPG and VVGPGA were able to raise KI67 protein expression in both test cell lines, according to a more detailed review. The P53, ATM, and SHH gene expression in the A549 cells increased to 19. 0 percent, 20. 7 percent, and 28. 77 percent, respectively. Interestingly, the VGVAPG peptide had an effect on the expression of antioxidant enzymes SOD2 and CAT in the A549 and MCF-7 cells, particularly after the 24-h treatment. Both A549 and MCF-7 cells' cells are affected by the tested EDPs at the cellular level, according to our findings.

Source link: https://europepmc.org/article/MED/35598370


Biphasic dose-dependent G0/G1 and G2/M cell cycle arrest by synthetic 2,3-arylpyridylindole derivatives in A549 lung cancer cells.

"About a sample of 2,3-arylpyridylindole derivatives were synthesized by the Larock heteroannulation and tested for their in vitro cytotoxicity against A549 human lung cancer cells. " Two derivatives demonstrated good cytotoxicity in vitro, with IC 50 values of 1. 18. 25 u00b10. 10 u03bcM and 0. 87 u00b10. 10u00b10. 10 u03bcM and inhibited tubulin polymerization in vitro, with molecular docking studies establishing the binding modes of the compounds in the colchicine binding site, according to molecular docking studies.

Source link: https://europepmc.org/article/MED/35595678


Induction of A549 Nonsmall-Cell Lung Cancer Cells Proliferation by Photoreleased Nicotine.

"In the present review, we show that RuBi-caged nicotine can be used as a source of free nicotine to promote proliferation of A549 non-cell lung cancer cells by acting on nicotinic acetylcholine receptors present in these cells. " During 72 h of cell culturing, RuBi-nicotine produced 2 bcm [Nic] p/r, which increased A549 cell proliferation in a similar manner to the 2 u03bcm of plain nicotine during 72 h of cell culturing. We conclude that RuBi-nicotine can be a useful source of free nicotine for inducing short- and long-term biological effects. ".

Source link: https://europepmc.org/article/MED/35569087

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions