Both, inositol 1,4,5-trisphosphate receptor type 1 (IP<sub>3</sub>R1) and type 1 sodium calcium exchanger (NCX1) were upregulated due to nifedipine in DLD1 and A2780 cells, but not in breast cancer MDA-MB-231 and JIMT1 cells.
Bioinformatics prediction and experimental validation of a novel microRNA: hsa-miR-B43 within human CDH4 gene with a potential metastasis-related function in breast cancer.
In addition, ectopically expression of FOXN4 led to the decreased cell proliferation, reduced colony formation and metastatic abilities (EMT, migration and invasion) in breast cancer cell lines.
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.
The findings of this study show that SNHG3 functions as an oncogene in breast cancer and promotes breast cancer cell proliferation and invasion by regulating the miR-384/HDGF axis.
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.
In the present study, we examined the anti-cancer effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin using a breast cancer model.
These results revealed that GAS6-AS2 sponges miR-493 to enhance the malignant characteristics of BC in vitro and in vivo by increasing FUT4 expression.
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.
Bioinformatics analyses suggested that <i>rs58450758</i> changes miR-559 secondary structure and forms new DICER sites in the pre-miRNA.<b>Conclusion</b>: The miR-559 <i>rs58450758</i> variant is linked to breast cancer.
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.
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.
In conclusion, the results of the present study identified a novel lncRNA PSMG3‑AS1, which serves as a sponge for miR‑143‑3p in the pathogenesis of breast cancer.
Both, inositol 1,4,5-trisphosphate receptor type 1 (IP<sub>3</sub>R1) and type 1 sodium calcium exchanger (NCX1) were upregulated due to nifedipine in DLD1 and A2780 cells, but not in breast cancer MDA-MB-231 and JIMT1 cells.