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Updated: Jan 25, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
LINC00511 knockdown enhances paclitaxel cytotoxicity in breast cancer via regulating miR-29c/CDK6 axis
Hualong Zhang1, Bin Zhao1, Xiuxia Wang2
1Department of Breast and Thyroid Surgery, Shanxian Central Hospital, Heze 274300, China.
Aims:
Drug resistance is becoming a major clinical challenge to the success of breast cancer treatment. Compelling evidence has shown the association between the deregulated long non-coding RNAs (lncRNAs) and drug resistance in various malignancies. However, the effects of long intergenic noncoding RNA 00511 (LINC00511), a newly identified oncogenic lncRNA, on the drug resistance of breast cancer cells remain unknown.
Main Methods:
RT-qPCR was performed to detect the expressions of LINC00511, miR-29c, and cyclin dependent kinase 6 (CDK6) in breast cancer tissues and cells. Pearson correlation analysis was used to analyze the correlation between miR-29c, CDK6 and LINC00511 expression in breast cancer tissues. The interactions between LINC00511, CDK6 and miR-29c were explored by luciferase reporter assay, RT-qPCR and western blot. MTT assay and flow cytometry analysis were applied to evaluate paclitaxel cytotoxicity.
Key Findings:
LINC00511 and CDK6 were upregulated while miR-29c was downregulated in breast cancer tissues and cells. miR-29c was negatively correlated with LINC00511 and CDK6 expression while LINC00511 was positively correlated with CDK6 expression in breast cancer tissues. LINC0051 directly interacted with miR-29c to suppress its expression. LINC00511 knockdown enhanced paclitaxel cytotoxicity in breast cancer cells by upregulating miR-29c. CDK6 was identified as a target of miR-29c. CDK6 knockdown attenuated the effects of miR-29c inhibition on paclitaxel cytotoxicity in breast cancer cells. LINC00511 positively regulated CDK6 expression in breast cancer cells.
Significance:
LINC00511 knockdown enhanced paclitaxel cytotoxicity in breast cancer cells via regulating miR-29c/CDK6 axis.
Insights
Long intergenic noncoding RNA 00511 (LINC00511) knockdown boosts paclitaxel efficacy in breast cancer by upregulating miR-29c and downregulating CDK6. This study reveals LINC00511 as a potential therapeutic target for overcoming drug resistance.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Drug resistance is a significant clinical challenge in breast cancer treatment.
- Long non-coding RNAs (lncRNAs) are implicated in cancer drug resistance.
- The role of LINC00511 in breast cancer drug resistance is currently unknown.
Purpose of the Study:
- To investigate the effect of LINC00511 on the drug resistance of breast cancer cells.
- To elucidate the molecular mechanism underlying LINC00511's role in breast cancer drug resistance.
Main Methods:
- Gene expression analysis (RT-qPCR) of LINC00511, miR-29c, and CDK6 in breast cancer tissues and cells.
- Correlation analysis between gene expressions.
- Luciferase reporter assays, RT-qPCR, and Western blot to explore molecular interactions.
- MTT assays and flow cytometry to assess paclitaxel cytotoxicity.
Main Results:
- LINC00511 and CDK6 were upregulated, while miR-29c was downregulated in breast cancer.
- LINC00511 directly suppressed miR-29c expression, and LINC00511 positively regulated CDK6.
- Knockdown of LINC00511 enhanced paclitaxel cytotoxicity by upregulating miR-29c.
- CDK6 was identified as a direct target of miR-29c.
Conclusions:
- LINC00511 knockdown enhances paclitaxel cytotoxicity in breast cancer cells.
- The mechanism involves the regulation of the miR-29c/CDK6 axis by LINC00511.
- LINC00511 is a potential therapeutic target for overcoming paclitaxel resistance in breast cancer.
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