LINC00680 modulates docetaxel resistance in breast cancer via the miR-320b/CDKL5 axis

Introduction: Increasing evidence has indicated that LINC00680 represents an oncogenic factor in cancer; however, the mechanism by which LINC00680 contributes to breast cancer (BC) remains unknown. Methods: A dual-luciferase reporter assay was used to explore the relationship between LINC00680, miR-...

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Published in:International journal of immunopathology and pharmacology 2022-05, Vol.36, p.3946320221105608-3946320221105608
Main Authors: Li, Jia, Ke, Jing, Qin, Cheng-lin, Zhu, Xun
Format: Article
Language:English
Subjects:
Bioinformatics
Breast cancer
Breast Neoplasms - drug therapy
Breast Neoplasms - genetics
Breast Neoplasms - metabolism
Cell proliferation
Cell Proliferation - genetics
Cholecystokinin
Cyclin-dependent kinase
Cyclin-dependent kinase 5
Cyclin-Dependent Kinase 5 - genetics
Cyclin-Dependent Kinase 5 - metabolism
Cyclin-dependent kinases
Docetaxel - pharmacology
Docetaxel - therapeutic use
Drug resistance
Drug Resistance, Neoplasm - genetics
Female
Gene Expression Regulation, Neoplastic - genetics
Humans
Kinases
MicroRNAs - genetics
MicroRNAs - metabolism
Original
Protein Serine-Threonine Kinases
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Summary:Introduction: Increasing evidence has indicated that LINC00680 represents an oncogenic factor in cancer; however, the mechanism by which LINC00680 contributes to breast cancer (BC) remains unknown. Methods: A dual-luciferase reporter assay was used to explore the relationship between LINC00680, miR-320b, and cyclin-dependent kinase 5 (CDKL5). A CCK-8 assay and transwell assay were utilized to evaluate the proliferation and invasion in docetaxel-resistant BC cells, respectively. Results: LINC00680 and CDKL5 protein levels were both upregulated when induced by different concentrations of docetaxel. LINC00680 knockdown decreased the expression level of drug resistance-related genes, proliferation, and invasion of BC cells. Bioinformatics prediction and dual-luciferase assays revealed that miR-320b targeted the 3′-unstranslated regions (UTR) of both LINC00680 and CDKL5, suggesting that the modulation of LINC00680 on CDKL5 occurred via sequestering miR-320b. Conclusion: Overall, this study highlights the important role of LINC00680 in docetaxel resistance through the miR-320b/CDKL5 pathway and provides a novel therapeutic strategy for BC drug resistance.
ISSN:0394-6320
2058-7384
DOI:10.1177/03946320221105608