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Published on: December 26, 2016
The synergistic effect of CDKN2B-AS1 and SPC25 on triple-negative breast cancer
Na Deng1,2, Keyan Chen3, Hua Fan2
1Department of Breast Surgery, The First Hospital of China Medical University, Shenyang, China.
Background:
Accumulating evidence suggests that long non-coding ribonucleic acid (RNA) cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) and messenger RNA (mRNA) spindle component 25 (SPC25) contribute to tumorigenesis and progression in various cancers. However, the synergistic effect between CDKN2B-AS1 and SPC25 has not yet been fully elucidated in triple-negative breast cancer (TNBC). This study sought to examine the synergistic effect of CDKN2B-AS1 and SPC25 and uncover a novel mechanism for the progression of TNBC.
Methods:
The transcriptome profiles of TNBC in The Cancer Genome Atlas (TCGA) were calculated for differentially expressed genes (DEGs). Gene co-expression networks were constructed via a weighted correlation network analysis. We validated the relationship between CDKN2B-AS1 and SPC25 by bioinformatics and in-vitro studies (including Cell Counting Kit-8, transwell assays, and quantitative real-time polymerase chain reaction).
Results:
CDKN2B-AS1 was found to be carcinogenic and was significantly upregulated and co-expressed with elevated SPC25 expression levels in the TNBC cells and sequencing profiles. Notably, the SPC25 mRNA levels were associated with poor clinical outcomes in TNBC patients. Specifically, the knockdown of CDKN2B-AS1 significantly inhibited TNBC cell proliferation and migration.
Conclusions:
We identified a novel cancer-promoting regulation axis. The co-expression of CDKN2B-AS1 and SPC25 is expected to serve as a powerful candidate biomarker for diagnostic and prognostic purposes in TNBC.
Insights
Long non-coding RNA CDKN2B-AS1 and mRNA SPC25 promote triple-negative breast cancer (TNBC) progression. Their co-expression serves as a potential biomarker for TNBC diagnosis and prognosis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNA (lncRNA) CDKN2B-AS1 and messenger RNA (mRNA) SPC25 are implicated in cancer development.
- The synergistic role of CDKN2B-AS1 and SPC25 in triple-negative breast cancer (TNBC) remains underexplored.
- Understanding this interaction may reveal novel therapeutic targets for TNBC.
Purpose of the Study:
- To investigate the synergistic effect of CDKN2B-AS1 and SPC25 in TNBC.
- To elucidate the underlying mechanism of TNBC progression driven by this axis.
- To evaluate the potential of CDKN2B-AS1 and SPC25 as biomarkers for TNBC.
Main Methods:
- Transcriptome analysis of TNBC using The Cancer Genome Atlas (TCGA) data.
- Weighted gene co-expression network analysis to identify gene interactions.
- In vitro validation including cell proliferation, migration assays, and qRT-PCR.
Main Results:
- CDKN2B-AS1 was identified as carcinogenic and significantly upregulated in TNBC.
- Elevated SPC25 expression was co-expressed with CDKN2B-AS1 and correlated with poor prognosis in TNBC patients.
- Knockdown of CDKN2B-AS1 suppressed TNBC cell proliferation and migration.
Conclusions:
- A novel cancer-promoting regulatory axis involving CDKN2B-AS1 and SPC25 was identified in TNBC.
- The co-expression of CDKN2B-AS1 and SPC25 shows promise as a diagnostic and prognostic biomarker for TNBC.
- This axis represents a potential therapeutic target for TNBC treatment.
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