Erratum: [Corrigendum] MicroRNA­23a inhibits endometrial cancer cell development by targeting SIX1.

[This corrects the article DOI: 10.3892/ol.2019.10694.].

MicroRNA-23a inhibits endometrial cancer cell development by targeting SIX1.

The present study focused on exploring the inhibitory mechanism of microRNA (miR)-23a in endometrial cancer. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to investigate miR-23a expression in endometrial tissues and endometrial cancer cells. A colony formation assay using crystal violet staining was performed to compare cell proliferation, while wound-healing and Transwell assays were performed to compare cell migration and invasion. Subsequently, bioinformatics and a luciferase reporter gene assay were used to investigate the effect of miR-23a on sine oculis homeobox homolog 1 (SIX1) expression, and the biological function of SIX1 was analyzed. Additionally, a nude mouse tumorigenicity assay was performed to test the inhibitory effect of miR-23a and Taxol® therapy in endometrial cancer. Finally, immunohistochemistry and RT-qPCR were used to explore the association between miR-23a and SIX1 expression in endometrial cancer tissues. miR-23a was underexpressed in endometrial cancer tissues compared with in para-carcinoma tissues, and the overexpression of miR-23a inhibited proliferation and invasion of endometrial cancer cells. Furthermore, SIX1 was demonstrated to be a downstream target of miR-23a, and miR-23a reduced SIX1 expression. Additionally, SIX1 inversely promoted cell proliferation, migration and invasion. In addition, the effects of reduced cell proliferation and increased cell invasion following miR-23a overexpression could be reversed by adding SIX1 to in vitro culture. Furthermore, the inhibitory effect of miR-23a and Taxol therapy, which reduced SIX1 expression in endometrial cancer, was demonstrated in vivo. Finally, a negative association between miR-23a and SIX1 expression was demonstrated in endometrial cancer tissues. The results of the present study revealed that miR-23a may inhibit endometrial cancer development by targeting SIX1.

The Increased PTK7 Expression Is a Malignant Factor in Cervical Cancer.

Cervical cancer is one of the most common malignant neoplasms in gynecology. Protein tyrosine kinase 7 (PTK7) with an inactive kinase domain is an important regulator of multiple Wnt pathways under normal and various pathological conditions and overexpressed in various tumors; however, the clinical and biological significance of PTK7 in cervical cancer is still unknown. In the present study, the protein expression level of PTK7 was detected in clinical cervical cancer patient samples, and the relationship between PTK7 expression and clinicopathological features was analyzed. In addition, the Kaplan-Meier method was performed to estimate the overall survival (OS) and progression-free survival (PFS) of patients to investigate the clinicopathological significance of PTK7 expression. Functional assays demonstrated that knocking down PTK7 might inhibit the ability of cancer cells to proliferate and invade or migrate, both in vivo and in vitro. Thus, PTK7 might serve as a potential target for cervical cancer.

Effect of nutritional supplement combined with exercise intervention on sarcopenia in the elderly: A meta-analysis.

OBJECTIVES: This systematic review was conducted to explore whether nutritional supplement can improve the benefits of exercise intervention on sarcopenia in the elderly. METHODS: Databases, including PubMed, Embase, Cochrane Library, Web of Science, CINAHL, CBM, CNKI, WANFANG, and VIP, were searched. All related papers with randomized controlled trials (RCT) methodology that were included in the databases from inception to 19 July 2016 were selected for the study. The tool "assessing risk of bias" from Cochrane Handbook 5.10 was used to evaluate the quality of included papers. A meta-analysis of eligible studies was performed using Stata12.0. Data that we were unable to convene or merge were subjected to descriptive analysis. RESULTS: Six trials were included in our study, which included 429 elderly patients with sarcopenia. The overall methodological quality of the trials was moderate. Compared with the exercise group, patients who were given nutritional supplements gained a bigger boost in fat-free mass (standard mean difference (SMD) = 5.78, 95% CI: 5.17 to 6.40, P = 0.000) and muscle mass (SMD = 2.048, 95% CI: 0.907 to 3.189, P = 0.000), as well as showed enhancement of keen extension strength (SMD = 1.08, 95% CI: 0.71 to 1.45, P = 0.000) and usual walk speed (SMD = 0.570, 95% CI: 0.19 to 0.95, P = 0.003). CONCLUSION: Nutritional supplementation may magnify the effect of exercise intervention on sarcopenia elderly in terms of muscle mass, muscle strength, and physical performance. Inconsistencies were present among research studies. More robust studies are needed to determine the most suitable type of nutrient and target population and to explore the actual role of combined intervention in managing sarcopenia in the elderly.