Product Description

Vincristine is an alkaloid that inhibits microtubule formation in the mitotic spindle, resulting in metaphase arrest of dividing cells. It exhibits antitumor activity and is used to treat various cancers, including leukemias, lymphomas, neuroblastoma, and Wilms' tumor.

Screeningbio‘s K562/Vincristine 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

Target Background

Vincristine (Oncovin) is a vinca alkaloid chemotherapeutic agent that binds to tubulin and inhibits microtubule polymerization, leading to disruption of mitotic spindle formation, cell cycle arrest at metaphase, and apoptosis in rapidly dividing cancer cells. It is widely used in the treatment of acute lymphoblastic leukemia, Hodgkin and non‑Hodgkin lymphomas, neuroblastoma, Wilms tumor, and other pediatric and adult malignancies. However, the development of drug resistance remains a major challenge limiting its long‑term efficacy.

Mechanistically, vincristine resistance arises through multiple cellular adaptations. Alterations in β‑tubulin isotypes (particularly class III β‑tubulin, TUBB3) or mutations in tubulin‑binding sites 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.