

K562 Paclitaxel Drug Resistance Cell
Item | Cat# | Price |
Drug Resistance Cell | SNB-G-0106A-H | Inquiry |
Compound Test Services | CT-002 | Inquiry |
Product Description
Paclitaxel is a chemotherapy drug used to treat various types of cancer, including breast, ovarian, lung, cervical, esophageal, and pancreatic cancer. It's also used to treat Kaposi's sarcoma, a type of cancer that causes abnormal tissue to grow under the skin in people with AIDS.
Paclitaxel is a taxane, a type of chemotherapy drug that prevents cancer cells from growing and dividing by interfering with microtubules, which help move chromosomes during cell division.
Screeningbio‘s K562/paclitaxel resistance cell line generated by exposing to increasing concentration of drug for certain period of time. After stable acquire resistance, cells were harvested and characterized for drug resistance by 7 days proliferation assay
Data
![Proliferation Assay. K562 and K562/Paclitaxel cell were seed at 384 well for 7 days proliferation assay. Paclitaxel was titrated for 11 point dose, 2 fold dilution. After 7 days compound treatment, cell was tested by CellTiter Glo reagent for viability test. Non-linear regression was used to plot viability changes vs. [Compound, nM], and IC50 values were determined, using GraphPad Prism software.](https://static.wixstatic.com/media/56275b_97cbf7ca6b5941628fcc0b1045db6dc1~mv2.png/v1/fill/w_75,h_75,al_c,q_85,usm_0.66_1.00_0.01,blur_2,enc_auto/56275b_97cbf7ca6b5941628fcc0b1045db6dc1~mv2.png)
Target Background
Paclitaxel (Taxol) is a widely used chemotherapeutic agent that stabilizes microtubules and inhibits mitotic spindle disassembly, leading to cell cycle arrest and apoptosis in rapidly dividing cancer cells. However, the development of drug resistance remains a major challenge limiting its long-term efficacy in various cancers, including breast, ovarian, and lung carcinomas.
Mechanistically, paclitaxel resistance arises through multiple cellular adaptations. Alterations in β-tubulin isotypes or mutations reduce drug binding affinity, while upregulation of efflux transporters such as P-glycoprotein (MDR1/ABCB1) decreases intracellular drug accumulation. Additionally, activation of survival pathways—including PI3K/Akt, MAPK, and NF-κB signaling—promotes anti-apoptotic responses. Changes in microtubule-associated proteins (MAPs) and enhanced autophagy or epithelial–mesenchymal transition (EMT) also contribute to reduced drug sensitivity.
Understanding these mechanisms is critical for designing strategies to overcome resistance, such as combination therapy with efflux inhibitors, targeting compensatory signaling networks, or employing patient-derived resistant cell models to guide personalized therapy development.