Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells
Background FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied. Methods The expression of FAM64A mRNA in BrC samples was determined...
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Veröffentlicht in: | Breast cancer (Tokyo, Japan) Japan), 2019-11, Vol.26 (6), p.835-845 |
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Sprache: | eng |
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Zusammenfassung: | Background
FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied.
Methods
The expression of
FAM64A
mRNA in BrC samples was determined by RT-qPCR assay and TCGA database mining. Kaplan–Meier plotter was used to analyze whether FAM64A expression impacted prognosis. Then, the expression of FAM64A was silenced using RNA interference. Cell-counting assay, colony formation assay and flow cytometry assay were conducted to detect proliferation; transwell migration assay, EMT-related proteins expression (E-cadherin, N-cadherin and vimentin), and EMT-related transcription factors mRNA expression (
Snail
,
Twist
,
Slug
) were conducted to evaluate the migration ability.
Results
FAM64A was highly expressed in human BrC samples, which was negatively associated with poor survival time. Analysis of FAM64A expression in BrC cell lines demonstrated that the expression of FAM64A was significantly correlated with the proliferation rate and migration ability of BrC cells. Indeed, knockdown of FAM64A suppressed the proliferation of MDA-MB-231 and MCF-7 cells. Importantly, we also found that silencing of FAM64A inhibited the migration of BrC cells via impeding epithelial–mesenchymal transition.
Conclusions
Our findings suggest that FAM64A plays an important role in the proliferation and migration of BrC cells, which might serve as a potential target for BrC treatment. |
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ISSN: | 1340-6868 1880-4233 |
DOI: | 10.1007/s12282-019-00991-2 |