Results showed that in northwest Chinese Han population, SNP rs17530068 (LOC105377871) increases the risk of breast cancer and SNP rs4784227 (CASC16) promotes lymph node metastasis in breast cancer patients.
Our results demonstrated that miR-3922-5p was a direct target of HOXC-AS3, and PPP1R1A was a target of miR-3922-5p in breast cancer.<b>Conclusions:</b> The novel lncRNA HOXC-AS3 acts as a miR-3922-5p sponge to upregulate PPP1R1A protein expression, and thus results in promoting breast cancer metastasis.
Moreover, molecular pathway enrichment analysis reveals that lack of CARMIL3 leads to loss of cell adhesions and low CARMIL3 expression in breast cancer patient specimens is implicated in epithelial-mesenchymal transition.
Receiver operating characteristic curve analyses indicated that miR‑150‑5p [area under the curve (AUC)=0.705, upregulated], miR‑576‑3p (AUC=0.691, upregulated), miR‑4665‑5p (AUC=0.681, upregulated) were able to distinguish breast cancer patients with recurrence from those without recurrence.
Here, we demonstrated that breast cancer (MDA-MB-231) cell-derived exosomes (231-Exo) could be specifically internalized by non-small cell lung cancer cells via a specific interaction between overexpressed integrin β4 (on exosomes) and surfactant protein C (SPC) on the cancer cells.
LINC00641 acts as a competitive endogenous RNA to sponge miR-194-5p. miR-194-5p level was higher in BC tissues and cells compared with normal-adjacent tissues and normal breast epithelial cell. miR-194-5p expression was negatively correlated with LINC00641 expression in BC tissues. miR-194-5p overexpression reversed the effects of LINC00641 on cell proliferation, cycle, apoptosis, migration, as well as invasion.
Taken together, our results demonstrate that ST7L exerts antitumor function in breast cancer associated with the suppression of Wnt/β-catenin signalling, suggesting ST7L as a potential therapeutic target for breast cancer.
In the present study, surface doses within the target area and contralateral breast (CLB) received during conventional treatment of carcinoma breast are evaluate and compared for treatment on two different beam energies, i.e., Co-60 γ-ray and 6 MV X-ray beams with thermoluminescent dosimeter, LiF:Mg, Ti (TLD-100).
For example, AF1q has been shown to interact with T-cell Factor 7 (TCF7; also known as TCF1) from the Wnt/β-catenin pathway resulting in the transcriptional activation of the CD44 and the enhancement of breast cancer metastasis.
Taken together, these evidences suggested that CERS6-AS1 promoted the progression of BC by binding to IGF2BP3 and thus enhancing the stability of CERS6 mRNA, providing a new underlying therapeutic target for BC to improve prognosis.