The effect of tibolone treatment on fasting blood sugar, insulin, insulin resistance and endothelial function in postmenopausal women: A meta-analysis of randomized controlled trials.

BACKGROUND AND AIM: The menopause is associated in females with the presence of dysglycemia, insulin resistance and with the development of endothelial dysfunction. Tibolone (TIB) is a synthetic steroid compound with selective oestrogenic and, to a lesser extent, progestogenic and androgenic properties prescribed to postmenopausal women to alleviate the symptoms of the climaterium and to prevent the development of osteoporosis. However, the impact of TIB on fasting blood sugar (FBS), insulin, Homeostatic Model Assessment-Insulin Resistance (HOMA-IR) index and flow-mediated dilation (FMD) in women has not been evaluated so far. Thus, to investigate this research question, we conducted the present systematic review and meta-analysis. METHODS: Two independent reviewers searched the Scopus, Web of Science, PubMed/Medline and Embase databases up to 20 December 2020. The weighted mean differences (WMDs) and the 95% confidence intervals (CI) were calculated using the DerSimonian and Laird random effects models between the TIB and control groups and included in the forest plot. RESULTS: The overall findings were generated from 12 eligible randomized controlled trials. As compared to controls, TIB administration resulted in a significant reduction of FBS (WMD: -3.06 mg/dL, 95% CI: -5.30 to -0.82, P = 0.007), and of the HOMA-IR index (WMD: -0.61, 95% CI: -1.11 to -0.11, P = 0.01). However, treatment with TIB did not lead to significant changes of the FMD (WMD: 0.78%, 95% CI: -0.20 to 1.77, P = 0.12) or of insulin levels (WMD: -0.10 mIU/L, 95% CI: -2.04 to 1.83, P = 0.91). CONCLUSION: TIB administration can decrease FBS and the HOMA-IR index in postmenopausal women. However, the use of TIB does not influence insulin levels or FMD.

LncRNA LINC01305 promotes cervical cancer progression through KHSRP and exosome-mediated transfer.

Cervical cancer (CC) is one of the deadliest female malignancies worldwide. Long non-coding RNAs (lncRNAs) are essential regulators for cancer progression. This study aimed to elucidate the role of lncRNA LINC01305 in the progression of CC. We found where LINC01305 was expressed in CC tissues and its correlation with the survival rate of CC patients. Functional experiments were performed to elucidate the effect of LINC01305 on CC. The results showed that LINC01305 was increased in CC tumor tissues and was correlated with a lower survival rate. The overexpression and knockdown of LINC01305 enhanced and inhibited the progression of CC, respectively. Additionally, the upregulation of LINC01305 promoted tumor growth in xenograft mice. Moreover, the effect of LINC01305 on CC was mediated through interacting with the RNA-binding protein, KHSRP. Furthermore, LINC01305 was mainly distributed in exosomes and was transferred to recipient cells to enhance CC progression. Lastly, LINC01305 may participate in the regulation of the stemness of CC. Taken together, the results suggest that LINC01305 promotes the progression of CC through KHSRP and that LINC01305 is released through exosomes and is involved in the stemness of CC. This study sheds light on the molecular mechanism underlying the progression of CC.