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pp.143-150
KX-01 (KX2-391or Tirbanibulin) is a reversible small-molecule inhibitor that binds to the colchicine-binding site of β-tubulin, leading to transient inhibition of microtubule polymerization. Although KX-01 has exhibited favorable pharmacologic properties and low toxicity in several epithelial malignancies, its therapeutic potential in salivary gland mucoepidermoid carcinoma (MEC) remains undefined. In this study, MC3 and YD15 MEC cells were exposed to KX-01 to assess its antitumor activity. Cell viability, anchorage-independent growth, and apoptotic morphology were examined using trypan blue exclusion, soft agar, and DAPI staining assays. Flow cytometric and immunoblot analyses were performed to quantify apoptotic cell populations and associated molecular markers. KX-01 treatment profoundly suppressed cell viability and colony formation, induced chromatin condensation and nuclear fragmentation, and markedly increased Annexin V–positive and sub-G1 populations. Furthermore, its enhanced cleavage of PARP and cleaved caspase-3. Collectively, these findings demonstrate that KX-01 exerts potent cytotoxic effects in MEC by triggering apoptotic pathway, supporting its further development as a targeted therapeutic candidate for human salivary MEC.
Ⅰ. INTRODUCTION
Ⅱ. MATERIALS and METHODS
1. Cell culture and reagents
2. Cell viability assay
3. Soft agar assay
4. Live/Dead assay
5. 4′-6-Diamidino-2-phenylindole (DAPI)staining
6. Annexin V/PI double staining
7. Cell cycle distribution analysis
8. Western blot analysis
9. Statistical analysis
Ⅲ. RESULTS
1. KX-01 reduces cell viability in MC3 andYD15 cells
2. KX-01 suppresses anchorage-independentgrowth and promotes cell death in MEC cells
3. KX-01 induces apoptotic nuclear morphologyand Annexin V–positive cell populations
4. KX-01 activates apoptotic signaling pathwaysby increasing cleaved PARP and cleavedcaspase-3 expression
Ⅳ. DISCUSSION
AKNOWLEDGEMENTS
REFERENCES
