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Xenograft Model Antitumor Assays / Lncrna / Cell Line, Tumor · Journal article
Cancer Biology & Therapy · May 26, 2026
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This is a mechanistic study combining TCGA database analysis with in vitro cell experiments demonstrating that long non-coding RNA AC008406.3 suppresses cuproptosis and reduces docetaxel efficacy in breast cancer cells. Knockdown of AC008406.3 enhanced docetaxel-induced cell death via cuproptosis pathway activation, but the work remains preclinical and lacks human clinical validation.
Integrated TCGA database analysis with in vitro mechanistic cell biology study. Breast cancer cell lines and TCGA-BRCA cohort; specific cell lines and cohort size not detailed in provided excerpt. Intervention: AC008406.3 knockdown and overexpression in breast cancer cells; docetaxel exposure. Compared with: Control cells without AC008406.3 manipulation; cells without docetaxel treatment. China (Wuhan and Tianjin institutions); TCGA data international.
AC008406.3 exhibited high expression in breast cancer samples associated with unfavorable prognostic outcomes AC008406.3 knockdown induced cuproptosis evidenced by increased intracellular copper levels and downregulation of lipoylated proteins and Fe–S cluster proteins AC008406.3 knockdown suppressed breast cancer cell proliferation, invasion, and migration
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This identifies a potential therapeutic target (AC008406.3) to enhance docetaxel sensitivity via cuproptosis induction, but findings are limited to cultured cells and require validation in animal models and clinical trials before clinical application.
In vitro and database study identifying lncRNA AC008406.3 as a cuproptosis regulator affecting docetaxel sensitivity in breast cancer cells, lacking clinical validation or human efficacy data.
As stated by the source record.
This identifies a potential therapeutic target (AC008406.3) to enhance docetaxel sensitivity via cuproptosis induction, but findings are limited to cultured cells and require validation in animal models and clinical trials before clinical application.
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Background. Docetaxel (DTX) is one of the commonly used chemotherapeutic agents for breast cancer. Cuproptosis, a newly defined form of cell death, significantly influences tumor progression. This study aims to identify cuproptosis-related long non-coding RNAs (lncRNAs) involved in regulating the sensitivity of breast cancer to DTX.Materials. Cuproptosis-related prognostic lncRNAs in breast cancer were identified through integrated co-expression, differential expression, and prognostic analyses based on the TCGA-BRCA cohort. The role of the identified lncRNA AC008406.3 in regulating cuproptosis in breast cancer cells was experimentally verified. The impact of DTX on the induction of cuproptosis was investigated, and rescue experiments were conducted to validate the involvement of AC008406.3 in modulating breast cancer sensitivity to DTX.Results. AC008406.3 was identified as a potential cuproptosis-related prognostic lncRNA in breast cancer, exhibiting high expression in breast cancer samples, which was associated with unfavorable prognostic outcomes. Knockdown of AC008406.3 specifically induced cuproptosis in breast cancer cells, as evidenced by increased intracellular copper levels and downregulation of lipoylated proteins and Fe-S cluster proteins, thereby suppressing cell proliferation, invasion, and migration; conversely, AC008406.3 overexpression elicited opposite phenotypic changes. Notably, DTX induced the occurrence of cuproptosis in breast cancer, whereas AC008406.3 suppressed this process, thereby diminishing DTX efficacy. However, AC008406.3 knockdown synergistically enhanced the anti-tumor efficacy of DTX in inhibiting breast cancer growth.Conclusion. AC008406.3 reduces the sensitivity of breast cancer to DTX by suppressing cuproptosis. Targeting AC008406.3 may represent a potential strategy to sensitize breast cancer cells to DTX.
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