Cervical cancer remains one of the most frequent gynecological malignancies among females around the world. Therefore, fully understanding the molecular mechanisms underlying the progression of cervical cancer may be critical for the development of effective therapeutic strategies against cervical cancer. The object was to evaluate the potential effect of miR-211 and verify its influence on the function of secreted protein acidic and rich in cysteine (SPARC) in cervical cancer. It was demonstrated that miR-211 was downregulated in cervical cancer cell lines (HeLa and C33A) and cervical cancer specimens, while SPARC expression level was higher in tumor tissues. We also revealed miR-211 upregulated expression could inhibit cells proliferation, migration and invasion in vivo. SPARC was confirmed as a direct and functional target of miR-211 and the inverse relationship between them was also observed. The results of the present study suggest that miR-211 reduced cancer growth, migration and invasion, and suppresses the SPARC expression in cervical cancer. This newly identified miR-211 may provide further insight into the progression and offers a promising target for cervical cancer therapy.
We believe this syndrome resulted from mytoxicity or perimuscular inflammation, producing contracture hypotropia and restricted elevation of the globe. We propose the term postbupivacaine hypotropia for this chiefly left-sided syndrome.
Background. This study aims to investigate the clinical efficacy of chemotherapy combined with traditional Chinese medicine in patients with cervical cancer and its effect on cellular immunoglobulin, serum sugar chain antigen 125 (CA125), carcinoembryonic antigen (CEA), and tumor necrosis factor-α (TNF-α). Methods. Conventional chemotherapy was performed in control and observation groups. Meantime, the observation group received traditional Chinese medicine. Finally, the clinical efficacy, immunoglobulin, serum tumor markers, and serum TNF-α of the two groups were compared. Results. Compared with the control group, total effective rate in the observation group was increased. After treatment, serum CD8+, TNF-α, CA125, and CEA levels were reduced in the two groups, and the observation group was higher. In the two groups, CD3+ and CD4+ levels were enhanced after treatment, and the observation group was also higher. Compared with the control group, the immunoglobulin IgG, IgA, and IgM levels increased in the observation group. The incidence of adverse reactions in the observation group was reduced compared to the control group. Conclusion. Chemotherapy combined with traditional Chinese can help improve the clinical efficacy and immunity in patients with cervical cancer. Moreover, the safety and feasibility of the treatment method are relatively high.
Objective
To investigate the possibility of microRNA (miR)‐337‐3p in the protection of hypoxia‐induced injury in PC12 cells via modulating the JAK2/STAT3 signaling pathway.
Methods
Dual‐luciferase reporter assay analyzed the relationship between the miR‐337‐3p and JAK2. PC12 cells were divided into normal, CoCl2, CoCl2 + NC, CoCl2 + inhibitors, CoCl2 + JAK2, and CoCl2 + mimics + JAK2 groups. Then, PC12 cell viability and apoptosis were measured by the 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) and Annexin‐V‐fluorescein isothiocyanate/propidium iodide methods. Quantitative real‐time polymerase chain reaction and Western blot analysis were used to determine expressions. Besides, the intracellular reactive oxygen species (ROS) was examined by dichloro‐dihydro‐fluorescein diacetate (DCFH‐DA) while the mitochondrial membrane potential (MMP) by using JC‐1.
Results
The negative targeting relationship between miR‐337‐3p and JAK2 was confirmed. When compared with the normal group, miR‐337‐3p was increased while JAK2 and STAT3 were decreased in CoCl2‐induced PC12 cells, with decreased cell viability. Moreover, either miR‐337‐3p inhibitor or JAK2 overexpression could partially reverse CoCl2‐induced decrease in PC12 cell viability. Besides, CoCl2 could also trigger PC12 cell apoptosis by increasing cleaved caspase 3 and Bax but decreasing Bcl‐2 and Bcl‐XL, which, however, were abolished with the transfection of miR‐337‐3p inhibitors or lentivirus transfection to activate JAK2. Compared with the CoCl2 group, the average of fluorescent signals of ROS in the CoCl2 + inhibitors group and the CoCl2 + JAK2 group was lower, while the activities of superoxide dismutase, catalase, glutathione peroxidase, and total anti‐oxidative capacity were higher, together with an increase in MMP.
Conclusion
Inhibiting miR‐337‐3p could activate the JAK2/STAT3 signaling pathway to suppress CoCl
2‐induced cytotoxicity and apoptosis and ameliorate oxidative stress and MMP in PC12 cells.
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