Aggressive forms of breast cancer are resistant to taxol chemotherapy. in these cancers, the gene encoding a protein called stathmin is overexpressed. to investigate the mechanism of action of stathmin, investigators measured tumor volume over time in mice with aggressive cancers under three conditions: no treatment (control), taxol treatment, and taxol treatment with stathmin gene expression turned off (taxol + δstathmin). their results are shown below. use these results to hypothesize how the stathmin protein affects microtubule stability.

The stathmin protein decreases the stability of microtubules. When stathmin is absent, the microtubule-stabilizing effect of taxol is enhanced, and the cells are more likely to arrest•Microtubules are found in cytoplasm of cell.•Microtubules form the cytoskeleton of the cell.•Microtubules form the spindle arrangement during cell division.•The spindle formation of microtubule helps in pulling chromosomes apart.•Microtubules can assemble or disassemble.•Tubulin is an important globular protein involved in assembly of microtubules.•Stathmin protein depolymerizes microtubule assembly through binding tubulin protein.•Due to stathmin-tubulin interaction, spindle formation gets arrested and thus cell cycle stops.•Generally, stathmin controls cell proliferation through checking spindle formation.•But here, in control as well as in taxol chemotherapy conditions, the stathmin is not at all acting in interruption of spindle and the cell division is continuous.•When these cancerous tumors treated with taxol under stathmin gene off conditions, the interruption of spindle formation can be seen and the cell cycle gets arrested.•The reason might be the stathmin protein might become mutated and not at all acting on interruption of cell division in control as well as taxol alone treated conditions.•This is due to production of stathmin in cancerous cells treated with taxol.

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