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A431 Cell - Crossref

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Last Updated: 10 June 2022

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Regulation of Bcl-2 Expression by HuR in HL60 Leukemia Cells and A431 Carcinoma Cells

"Expression of bcl-2 is determined, in part, by legislative mechanisms that maintain the stability of bcl-2 mRNA. " In vivo, HuR binds to bcl-2 mRNA. In addition, nucleolin and HuR bind simultaneously to bcl-2 AU-rich element RNA in vitro, establishing separate binding sites for these proteins on bcl-2 mRNA. In HuR knockdown cells, evidence of a decreased ratio of bcl-2 mRNA to heterogeneous nuclear RNA suggested a positive role for HuR in regulating bcl-2 stability. RNA isolateds of HL60 cells from recombinant HuR retards exosome-mediated degradation of bcl-2 ARE RNA in exosome-mediated decay of bcl-2 ARE RNA in exosome-mediated degradation. This supports HuR's involvement in the regulation of bcl-2 mRNA stability in HL60 cells as well as in A431 cells. "HuR appears to have a positive effect on both regulation of bcl-2 mRNA translation and mRNA stability. ".

Source link: https://doi.org/10.1158/1541-7786.mcr-08-0476


Regulation of Apoptosis Reduction in the Cisplatin-Resistant A431 Cell Line by Bcl-2 and CPP32

"Recent studies have shown that chemotherapy can promote apoptosis in certain cancer cells, indicating that apoptosis may play a major role in cancer therapy. " To determine whether apoptosis modulation modulates CDDP resistance, we used a CDDP-resistant cell line from the human epidermoid carcinoma cell line A431. In comparison to A431 cells treated with CDDP, the CDDP-resistant cell with DNA gel electrophoresis and ELISA showed reduced apoptosis and ELISA. This report revealed a marked rise in Bcl-2 protein levels as well as a decrease in CPP32 protein levels in CDDP-resistant cells.

Source link: https://doi.org/10.1159/000007258


Establishment and Characterization of Cisplatin-Resistant Human Epidermoid Carcinoma Cell Line, A431 Cell

"Cisplatin, cis-diamminedichloroplatinum, is one of the most commonly used anticancer drugs, initially showing positive results in a variety of tumors. " We also produced two CDDP-resistant sublines A431/CDDP1 and A431/CDDP2 from human epidermoid carcinoma cell line A431, which is also known as A431. In terms of IC50, the new A431 cell has shown 3. 2 and 2. 7 times more resistance to CDDP1 and A431/CDDP2 have grown 3. 1 and 2. 7 times more resistance to CDDP than the original A431 cell. Both CDDP analogue, carboplatin, was shown cross-resistance to the CDDP analogue, but not to other chemotherapeutic drugs such as Adriamycin and 5-fluorouracil. To demonstrate the sensitivity to CDDP treatment in vivo, these CDDP-resistant sublines were transplanted into nude mice. The mechanism of resistance in A431/CDDP1 and A431/CDDP2 seems to be based on a decrease in intracellular accumulation of CDDP, since their platinum concentration, the main component of CDDP, has significantly decreased," according to the in vitro assay.

Source link: https://doi.org/10.1159/000007153


Centipede Scolopendra suppresses cell growth in human epidermoid carcinoma cell A431

"The aim of this research was to investigate the anti-proliferation and migration effects of Centipede Scolopendra extracts on human epidermoid carcinoma cells A431 and determine the underlying signaling mechanisms. " By wound-healing assays and matrigel invasion chamber assays, migration and invasion potential of A431 cells was determined. CSE strengthened its anti-proliferation and anti-migration by targeting EGFR and associated metastasis genes, thereby making it a promising therapeutic candidate for high-EGFR expression cancer therapy.

Source link: https://doi.org/10.3329/bjp.v12i3.32525


Piezo1 activation using Yoda1 inhibits macropinocytosis in A431 human epidermoid carcinoma cells

"Ras-transformed cancer cells rapidly obtain exogenous amino acids for their survival by macropinocytosis. " In summary, inhibition of macropinocytosis is a promising therapy for cancer therapy. Yoda1's inhibition of ruffle formation was dependent on the extracellular Ca 2+ influx through Piezo1 and the initiation of the calcium-activated potassium channel KCa3. 1. This means that Ca 2+ ions will control EGF-stimulated macropinocytosis, according to this.

Source link: https://doi.org/10.1038/s41598-022-10153-8


Activation of calcium entry in human carcinoma A431 cells by store depletion and phospholipase C- dependent mechanisms converge on I CRAC -like calcium channels

"Activation of phospholipase C in nonexcitable cells leads to calcium leakage from intracellular stores and the activation of Ca 2+ migration by means of Ca 2+ release-activated channels in the plasma membrane. " The observed channels have the same conductance and gating characteristics as previously described I min channels, but have significantly lower conductance for monovalent cations than the I CRAC channels. Prolonged exposure of patches to thapsigargin renders I CRACL Ca 2+ channels unresponsive to IP 3 but also ready to activate by a combination of IP 3 and anti-PIP 2 antibodies. Based on these results, we found that phospholipase C-mediated and store-operated Ca 2+ influx pathways in A431 cells converge on the same I CRACL Ca 2+ channel, which can be modified by PIP 2. ".

Source link: https://doi.org/10.1073/pnas.98.1.148


Metabolic labeling of mitogen-activated protein kinase kinase in A431 cells demonstrates phosphorylation on serine and threonine residues.

"Mitogen-activated protein kinase is an enzyme that promotes the growth factor-regulated MAP kinase in vitro by a process that involves direct phosphorylation of MAP kinase on tyrosine and threonine residues. " The kinase is phosphorylated on serine and threonine residues, according to an analysis of two epidermal growth factor-stimulated MAP kinase cells, and serine dephosphorylation is correlated with serine and threonine phosphatase treatments resulting in serine dephosphorylation. ".

Source link: https://doi.org/10.1073/pnas.90.11.5143


Thiol protease-specific inhibitor E-64 arrests human epidermoid carcinoma A431 cells at mitotic metaphase.

Human epidermoid carcinoma A431 cells were arrested during mitotic metaphase by a membrane-permeant inhibitor E-64. Following the cell cycle analysis by flow cytometry, the relative proportion of the G2/M population increased 2. 5-fold after 5 hr of cell culture treatment. In addition, time-lapse video analysis revealed that E-64-treated cells remained at metaphase for an extended period after rounding-up, while untreated cells completed mitosis within 42. 0 +/- 5. 7 min. ".

Source link: https://doi.org/10.1073/pnas.85.1.146


Extracellular ATP is a mitogen for 3T3, 3T6, and A431 cells and acts synergistically with other growth factors.

"The percentage of cell nuclei labeled with [3H]thymidine and cell number had also increased. " In addition, it was found that ATP synergised in 3T6 and 3T3 cells during the first hour of an incorporation, though no significant hydrolysis occurred at that time. Besides, extended preincubation of cells with ATP decreased the mitogenic response to ATP but not to adenosine; preincubation with adenosine or N6-adenosine had the reverse effect. Extracellular ATP is a mitogen that interacts with P2 purinoceptors on the plasma membrane, and we conclude that we're right.

Source link: https://doi.org/10.1073/pnas.86.20.7904


Diphtheria toxin prevents catecholamine desensitization of A431 human epidermoid carcinoma cells.

According to respective, actinomycin D and cycloheximide have been used to inhibit RNA and protein synthesis in vivo and cytochrome. In A431 human epidermoid carcinoma cells, we also tested whether diphtheria toxin could prevent catecholamine-induced desensitization. Cellular cAMP results after a 30-min exposure to isoproterenol were similar in both control and toxin-treated cells. However, toxin-treated cells after 4 hours of isoproterenol therapy, results in up to six times more cAMP than controls. These findings reveal that diphtheria toxin, a specific inhibitor of protein synthesis, can interfere with cAMP metabolism in eukaryotic cells and provide convincing evidence that catecholamine stimulation of adenylate cyclase.

Source link: https://doi.org/10.1073/pnas.84.8.2246

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* 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