MiRNA-214 promotes the pyroptosis and inhibits the proliferation of cervical cancer cells via regulating the expression of NLRP3.

Inflammasome mediates the maturation of interleukin-1ß (IL-1ß) and IL-18, triggers the pyroptosis and associates with multiple autoimmune diseases. In light of this, we hope to investigate the regulatory role of miRNA-214 in the inflammasome of cervical cancer. With the samples collected from 50 cervical cancer patients and 50 age-matched healthy subjects, real-time PCR and Western blotting were employed to detect the mRNA and/or protein expression profiles of the NOD-like receptor protein family, including NLRP1, NLRP3, NLRC4, Caspase-1, IL-1ß, IL-18 and miR-214. Corresponding plasmids were used to transfect the Hela, HCC94, Siha or HUCEL normal cell lines to upregulate or downregulate the expression of targeted genes and to construct the cervical cancer models on rats. In addition, RT-PCR and Western blot were also considered to detect the expression of miR-214 and pyroptosis-related genes, while the pyroptosis of cells was evaluated by using the caspase-1 activity detection kit. Downregulation of miR-214 was found in the cervical cancer patients and the cervical cancer cell lines (** P <0.01), while overexpression of miR-214 could induce the pyroptosis of cervical cancer cell by targeting NLRP3. In cervical cancer patients, miR-214 and NLRP3 are downregulated, while upregulation of miR-214, by enhancing the expression of NLRP3, can advance the pyroptosis of cervical cancer cells. In addition, we, for the first time, clarify the correlation of cervical cancer with the miR-214 and NLRP3.

Umbilical cord blood cells regulate endogenous neural stem cell proliferation via hedgehog signaling in hypoxic ischemic neonatal rats.

Umbilical cord blood mononuclear cells (UCBMC) transplantation may improve hypoxia-induced brain injury in neonatal rats, but the mechanism is unclear. This study examines whether UCBMC promote neural stem cell (NSC) proliferation via the Sonic hedgehog (Shh) signaling pathway. The rats underwent left carotid ligation followed by hypoxic stress. UCBMC were transplanted 24h after hypoxia ischemia (HI), and immunohistochemistry, immmunoblotting, and morphology analyses were performed at different time points after transplantation. Increased numbers of NSCs were observed in the subventrical zone (SVZ) of the HI+UCBMC group, but these increases were attenuated by cyclopamine treatment. There were significant increases in Shh and Gli1 protein levels after transplantation in the HI group treated with UCBMC compared to HI rats treated with phosphate-buffered solution (PBS). Significantly more Gli1(+)DAPI(+) cells were observed in the SVZ of the HI+UCBMC group compared to the HI+PBS and N+UCBMC groups, but few Gli1(+)DAPI(+) cells were found in the SVZ of the HI+cyclopamine+UCBMC group. The HI+UCBMC group had significantly less neuronal loss in the cortex and CA1 sector of the hippocampus compared to the HI+PBS group, but more neuron loss was observed in the HI+cyclopamine+UCBMC group compared to HI+UCBMC. These results indicate that UCBMC may promote NSC proliferation and alleviate brain injury in HI neonatal rats via Shh signaling.