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Human papillomavirus (HPV) infection alone is not sufficient for development of cervical cancer and further risk factors are involved, however, the underlying mechanism remains to be elucidated. The authors previously used a microarray assay to reveal microR-20b (miR-20b) as a key node in the miRNA-mRNA network of cervical carcinoma. The present study demonstrated an increased expression of miR-20b in cervical carcinoma tissue. MiR-20b was regulated by HPV E6 oncoprotein in cervical cancer. Furthermore, miR-20b overexpression with mimics induced cell morphological alterations and the epithelial-mesenchymal transition. Treating cervical cancer cells with the miR-20b inhibitor decreased the migration and invasion of cervical cancer cells. Tissue inhibitor of metalloproteinase 2 (TIMP-2), a possible antagonist of matrix metalloproteinase 2, is a metastasis suppressor and predicted to be a potential target of miR-20b. Fluorescence signals were decreased on transducing HeLa cells with a TIMP-2 3′-untranslated region plasmid and miR-20b mimics compared with control. Finally, TIMP-2 was identified as a novel target of miR-20b and was demonstrated to be regulated by the HPV oncoprotein. In addition, miR-20b and TIMP-2 were involved in cell invasion regulated by HPV E6. The present study demonstrated a novel pathway of HPV/miR-20b/TIMP-2 during the process of invasion in cervical cancer cells.

Aims: Omentin-1 was proved to be associated with ischemic stroke clinical functional outcome. It also predicted carotid atherosclerosis among metabolic syndrome subjects and type 2 diabetes patients. Our aim was to examine the association of omentin-1 levels with carotid plaque instability and stenosis degree among ischemic stroke patients.Methods: A total of 173 acute ischemic stroke patients were included in this study. Serum omentin-1 levels were assayed. Carotid ultrasound examinations were performed to evaluate the carotid plaque instability and stenosis degree. Multivariable logistic analyses were used to examine the association of serum omentin-1 levels with carotid plaque instability and stenosis degree.Results: Ischemic stroke patients with unstable carotid plaque had significantly lower levels of serum omentin-1 than patients with stable plaque (53 [40.2–64.1] vs 61.8 [52.4–77.2] ng/ml, P < 0.01). Subjects in the highest tertile of serum omentin-1 levels had a 0.31-fold risk of having unstable plaque compared with those in the lowest tertile (P < 0.05), and its trend test was significant (P for trend = 0.03). The integrated discrimination improvement was significantly improved in predicting carotid plaque instability when omentin-1 data was added to the multivariable logistic regression model. No significant association was detected between omentin-1 and moderate-severe carotid stenosis or occlusion.Conclusions: Among ischemic stroke patients, higher omentin-1 levels were inversely associated with carotid plaque instability, but not associated with moderate-severe carotid stenosis or occlusion. Omentin-1 may represent a biomarker for predicting carotid plaque instability of acute ischemic stroke patients.

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Higher omentin-1 levels at baseline were negatively associated with poor functional outcome among ischemic stroke patients. Omentin-1 may represent a biomarker for predicting poor functional outcome of acute ischemic stroke patients.