GeneChip expression profiling identified OLFML2A as a potential therapeutic target in TNBC cells

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background An elevated level of olfactomedin-like-2A ( OLFML2A ) is unfavorable for female breast cancer patients. Patients with a high mRNA level of OLFML2A receive a poor prognosis. Therefore, we speculate that inhibiting the expression of this gene may be beneficial to breast cancer patients. We previously found that silencing the OLFML2A gene by using mRNA interference significantly inhibited proliferation and migration in triple-negative breast cancer (TNBC) cells. Methods Cell activity and proliferation were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Celigo analyses. Cell migration and invasion were determined by wound-healing and transwell invasion assays. The mechanism of the inhibition of a small hairpin RNA that targets OLFML2A (sh OLFML2A ) was determined by using a GeneChip array, real-time quantitative PCR (RT-qPCR), and western blot analysis. Results Gene silencing by sh OLFML2A induces apoptosis by promoting S phase arrest in TNBC cells. In addition, sh OLFML2A decreased the progression of epithelial-mesenchymal transition (EMT). Additionally, microarray analysis showed that sh OLFML2A significantly upregulated 428 genes and downregulated 712 genes. These significantly changed genes regulated DNA synthesis, chromosome alignment, microtubules and the cytoskeleton, cell movement, the cell cycle, cell necrosis, and apoptosis

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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