miR-885-3p expression

The authors' research data on the role of the above markers in regulation of this pathway in neuroblastoma are presented. The study of alterations in expression of microRNAs and genes involved in p53 pathway regulation will not only expand our understanding of the mechanisms of neuroblastoma pathogenesis but could substantiate new approaches for delineating risk groups and risk stratification of neuroblastoma patients as well as treatment optimization based on the genetic characteristics of the tumor.

Adding AsO to the gastric cancer cells could significantly inhibit miR-885-5p expression, while miR-885-5p in gastric cancer cells affected cell expression by targeted regulation, affecting cell proliferation. AsO may be used as a drug treatment program for gastric cancer, and mainly regulates the proliferation of gastric cancer cells by affecting the miR-885-5p/CDC73 target axis to participate in the development of gastric cancer.

However, miR-885-5p inhibitor or mimic reversed the effects of silent circSERPINA3 or overexpressed circSERPINA3. Collectively, circSERPINA3 promotes proliferation, migration, and invasion of LSCC cells by targeting miR-885-5p.

Our data elucidated that circPTPRM may play an oncogenic role in PTC through circPTPRM/miR-885-5p/DNMT3A axis.

TLR4 overexpression weakened the impacts of miR-885-3p on LPS-stimulated cell injury and NF-κB-MyD88 signaling. In conclusion, miR-885-3p can reduce LPS-induced 16HBE cell damage, via targeting TLR4 to suppress the NF-κB-MyD88 pathway.

miR-885-5p expression was decreased in cervical cancer, and downregulation of miR-885-5p promoted the progression of cervical cancer cells. MiR-885-5p may be an independent prognostic predictor and therapeutic target for treating cervical cancer.

It was found that TGEV open reading frame 3b (TGEV-ORF3b) suppressed Bcl-10 expression, activation of NF-κB pathway, and TNF-α production by uniquely up-regulated miR-885-3p expression. Overall, the results indicated that TGEV-ORF3b counteracted NF-κB pathway and TNF-α via regulating miR-885-3p and Bcl-10.

Our data indicate that the ATO/miR-885-5p/MTPN axis may serve as a target for improving the sensitivity of CCA cells to chemotherapy.

Overexpression of miR-885-5p negatively regulates ME1 and causes changes in downstream molecules Vimentin and Fibronectin. Our research found that miR-885-5p plays a tumor suppressor gene and could potentially serve as a biomarker and therapeutic target in GC.

The results revealed that the TNM stage, lymphatic invasion, distal metastasis and miR-885-5p were independent prognostic factors affecting their 5-year survival. It was concluded that miR-885-5p exhibited the potential to be a serum biomarker to evaluate the efficacy of advanced liver cancer.