H69AR Whole Cell Lysate: sc-364382

H69AR whole cell lysate is derived from the H69AR cell line, which originates from the H69 human small cell lung carcinoma line but has been selected for resistance to the chemotherapy drug doxorubicin (Adriamycin). This lysate is extensively used in cancer research to understand the mechanisms of drug resistance, a significant challenge in cancer treatment. Researchers utilize H69AR lysate to study the cellular and molecular adaptations that confer resistance to chemotherapeutic agents, focusing on the overexpression of drug efflux pumps such as P-glycoprotein (P-gp), a product of the MDR1 gene, which actively transports drugs out of cells, reducing their cytotoxic effects. The lysate is instrumental in examining alterations in cell cycle regulation, apoptosis pathways, and DNA repair mechanisms in drug-resistant cells. Studies often focus on signaling pathways such as PI3K/Akt and MAPK/ERK, which are implicated in cell survival and proliferation. By comparing the protein expression profiles and post-translational modifications between H69AR and parental H69 cells, researchers can identify key molecular differences that contribute to the drug-resistant phenotype. Using H69AR whole cell lysate, scientists gain valuable insights into the cellular responses to chemotherapeutic stress and the genetic and epigenetic changes associated with acquired drug resistance.

H69AR Whole Cell Lysate References:

1. Biochemical characterization and NMR studies of the nucleotide-binding domain 1 of multidrug-resistance-associated protein 1: evidence for interaction between ATP and Trp653.  |  Ramaen, O., et al. 2003. Biochem J. 376: 749-56. PMID: 12954082
2. Non-P-glycoprotein-mediated multidrug resistance in a small cell lung cancer cell line: evidence for decreased susceptibility to drug-induced DNA damage and reduced levels of topoisomerase II.  |  Cole, SP., et al. 1991. Cancer Res. 51: 3345-52. PMID: 1675932
3. Infection of H69AR cells with retroviral particles harboring interfering RNAi significantly reduced the multidrug resistance of these small cell lung cancer cells.  |  Palaniyandi, K., et al. 2011. Int J Biochem Mol Biol. 2: 155-167. PMID: 21968975
4. MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway.  |  Tripathi, SC., et al. 2017. Cancer Res. 77: 4414-4425. PMID: 28646020
5. Linc00173 promotes chemoresistance and progression of small cell lung cancer by sponging miR-218 to regulate Etk expression.  |  Zeng, F., et al. 2020. Oncogene. 39: 293-307. PMID: 31477834
6. Reduced levels of topoisomerase II alpha and II beta in a multidrug-resistant lung-cancer cell line.  |  Evans, CD., et al. 1994. Cancer Chemother Pharmacol. 34: 242-8. PMID: 8004758