ArticleBreast cancer research : BCR2025
Investigating the mechanism of inositol against paclitaxel chemoresistance on triple-negative breast cancer by using 7T multiparametric MRI and mitochondrial changes.
Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Unlocking synergistic potential: enhancing paclitaxel efficacy in combination with silibinin in breast cancer cell line through H19 LncRNA and P53/Bax/Bcl2 axis.Annals of medicine and surgery (2012) · 2026Article
- The multifaceted roles of mitochondria and their therapeutic transformation: a new perspective on triple-negative breast cancer treatment.Frontiers in oncology · 2026Article
- IP6: From Seeds to Science-A Natural Compound's Path to Clinical Promise.Biomolecules · 2025Review
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11 authors.
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Abstract
backgroundThe emerging triple-negative breast cancer (TNBC) treatments target mitochondrial fission to combat paclitaxel (PTX) resistance. Inositol's inhibition of this process makes it a potential therapy. Multiparametric MRI provides an early and effective assessment of these innovations.
objectiveTo monitor the efficacy of Inositol on PTX-resistant TNBC mice using 7T multiparametric MRI, and to further explore the mechanism of inositol inhibiting PTX chemoresistance in combination with the morphological changes of isolated mitochondria. MATERIALS AND
methodsBALB/c mice aged 6-8 weeks were subcutaneously inoculated with PTX-resistant 4T1 cells and divided into three groups: PTX-treated mice (n = 24), "PTX + Inositol"-treated mice (n = 24) and untreated mice (n = 24). Six mice in each group underwent diffused weighted imaging (DWI) and diffusion kurtosis imaging (DKI) every 7 days after administration. To observe the dynamic changes of inositol within the tumor tissue post-treatment, chemical exchange saturation transfer (CEST) imaging was performed. Six mice in each group were sacrificed on day 0, 7, and 14 respectively for histopathological examination. After a 3-week scanning cycle, the remaining mice in each group were euthanized for histopathological analysis. The therapeutic response of inositol was assessed via Hematoxylin & Eosin (H&E) staining and Ki-67 immunohistochemistry. The effects of inositol on mitochondrial structure and PTX resistance were studied by Western Blot and electron microscopy. One-way analysis of variance, independent samples t-test, paired samples t-test, Kruskal-Wallis, and Spearman rank correlation were used.
resultsThe CEST signal of inositol in tumor tissue was significantly higher after 1 h of inositol administration than before (2.75 ± 0.71% vs. 1.80 ± 0.33%, p < 0.05). On day 21 after treatment, the tumor volume in the PTX + Ins group was smaller than that in the PTX group (191.52 ± 27.98 mm
conclusionInositol may counteract PTX resistance in TNBC by disrupting mitochondrial fission, and DWI combined with DKI effectively tracked this effect.
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