English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

microRNAs (miRNAs) have been demonstrated to play crucial roles in tumorigenesis. However, the molecular mechanism underlying the roles of miRNAs in breast cancer remains largely unknown. In this study, we showed that miR-335 is downregulated in a number of breast cancer tissues and cell lines. Luciferase reporter assays identified the paired box 6 gene (PAX6) as a novel target of miR-335. Further investigation revealed that miR-335 negatively regulates the expression of PAX6 in human breast cancer MCF-7 cells. Our results further suggested that overexpression of miR-335 inhibits MCF-7 cell proliferation by inducing cell-cycle arrest at the G1 phase via targeting PAX6. Western blot analysis showed that overexpression of miR-335 promotes p27 protein expression but inhibits cyclin D1 expression in MCF-7 cells; however, overexpression of PAX6 decreased the p27 protein level but increased the cyclin D1 protein level in MCF-7 cells. Furthermore, miR-335 overexpression reduced colony formation and cellular invasion in MCF-7 cells, an effect that was reversed by PAX6 overexpression. In conclusion, this study provides novel insights into the in vitro regulatory patterns of miRNA-335 and PAX6 in breast cancer, and indicates that miRNA-335 may constitute a promising candidate for the treatment of breast cancer.

microRNA-335 inhibits proliferation, cell-cycle progression, colony formation, and invasion via targeting PAX6 in breast cancer cells