For mechanism investigation, hsa_circ_0001038 could sponge miR-337-3p to release its suppression on cyclin-M3 (CNNM3) and metastasis-associated in colon cancer 1 (MACC1), thereby promoting CC cell growth and invasive potential, respectively.
These results indicate that ultrasound-mediated PTX-miR-34a-MBs synergistically inhibit the growth of cervical cancer via the upregulation of miR-34a and downregulation of Bcl-2 and CDK6.
We compared miR-21 and Smad7 levels in human samples from chemoradiotherapy-resistance cervical cancer (resistant group) and chemoradiotherapy-sensitive cervical cancer (sensitive group) patients.
The effects of CRNDE on the CC biological functions and CCNB1 expression were detected by conducting in virto and in vivo experiments. qRT-PCR, western blot and dual-luciferase reporter assay were used to predict the target of miR-183.
The overexpression of miR‑411 and low expression of STK17A were correlated with high efficacy of radiotherapy. miR‑411 and STK17A had predictive value for the efficacy of radiotherapy; miR‑411 was the protective factor and STK17A was a risk factor for prognosis of cervical cancer.
Our findings provide a better understanding of the molecular mechanism underlying circAMOTL1 in cervical cancer and indicated circAMOTL1/miR-485-5p/AMOTL1 as a promising novel therapeutic strategy for the treatment of this disease.
Based on sequencing data mining, we predicted that MBNL1 might be involved in the occurrence and poor prognosis of cervical cancer, and verifed that MBNL1 could regulate the resistance of HeLa cells to cisplatin via Nrf2.
The preliminary report revealed that the SNP rs4846048 of MTHFR enhanced the risk of CC through association with miR-522, which further regulated cell viability and apoptosis in Hela cells.