[Clinical observation of combined oral contraceptives drospirenone and ethinylestradiol tablets (â ¡) in the treatment of dysmenorrhea in Chinese women].

Objective: To evaluate the efficacy and safety of drospirenone and ethinylestradiol tablets (Ⅱ) in Chinese women with dysmenorrhea. Methods: This was a single-arm, open-label, interventional, multicenter, post-authorization safety/effectiveness study of drospirenone and ethinylestradiol tablets (Ⅱ) across 6 treatment cycles, a total of 526 patients were included in the dysmenorrhea subgroup. Visual analog scale (VAS) was used to assess the severity of menstrual pain. Secondary outcomes included unintended pregnancies, bleeding pattern, cycle control and safety. Results: After treated with drospirenone and ethinylestradiol tablets (Ⅱ), VAS of pain had decreased significantly compared with baselines [(49.5±23.7) vs (32.3±24.9) vs (20.7±19.4) vs (18.4±18.7) mm, P<0.01]. From the second cycle to the fifth cycle, the incidence of scheduled bleeding increased from 93.9% (450/479) to 96.4% (431/447). The duration of scheduled bleeding decreased from (5.7±2.7) to (5.4±1.8) days. The incidence of intermenstrual bleeding decreased from 9.0% (43/479) to 5.6% (25/447). 17.5% (92/526) patients reported adverse drug reactions, most frequently reported adverse events were breast pain, nausea, breast swelling, headache, and uterine bleeding. No death occurred during the study. Conclusion: Drospirenone and ethinylestradiol tablets (Ⅱ) is effective for the treatment of dysmenorrhea and has good safety.

LINC00205, a YY1-modulated lncRNA, serves as a sponge for miR-26a-5p facilitating the proliferation of hepatocellular carcinoma cells by elevating CDK6.

OBJECTIVE: LINC00205, a bidirectional lncRNA, located at human chromosome 21q22.3, was recently characterized as an oncogenic molecule contributing to cell proliferation in several cancers, including hepatocellular carcinoma (HCC). In the present study, we aim to probe the new molecular mechanism for LINC00205 controlling the proliferation of HCC cells. PATIENTS AND METHODS: The expression status of LINC00205, miR-26a-5p, as well as CDK6 in HCC tissues/cell lines was determined by quantitative real-time PCR (qPCR). The cell proliferative activity was measured by using the Cell Counting Kit (CCK)-8 assay. Flow cytometry was performed to analyze cell cycle progression and apoptosis induction. The interaction among LINC00205, miR-26a-5p and CDK6, as well as transcription efficiency of LINC00205 promoter were examined by Dual-Luciferase reporter assay. Western blot was conducted to evaluate the protein levels of CDK6 in SNU-449 cells. The direct interplay between YY1 and LINC00205 promoter was detected by ChIP-qPCR. RESULTS: LINC00205 was strongly expressed in HCC tissues and cell lines. Elevated LINC00205 expression was positively associated with worse prognosis as well as pathological grade in HCC. Suppression of LINC00205 could impede the proliferation of HCC cells by triggering the G0/G1-phase cell cycle arrest and apoptosis in vitro. Mechanistically, we illustrated that LINC00205 could accelerate the proliferation of HCC cells by boosting CDK6 expression via sponging miR-26a-5p. Moreover, we unveiled that LINC00205 could be activated by transcription factor Yin Yang-1 (YY1) as its direct downstream target. CONCLUSIONS: LINC00205, a novel YY1-modulated lncRNA, can facilitate the proliferation of HCC cells through YY1/miR-26a-5p/CDK6 pathway, and may serve as a promising diagnostic biomarker and therapeutic target for HCC.

Long noncoding RNA LINP1 promoted proliferation and invasion of ovarian cancer via inhibiting KLF6.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA LINP1 promoted proliferation and invasion of ovarian cancer via inhibiting KLF6, by Y. Li, C.-Z. Hou, Y.-L. Dong, L. Zhu, H. Xu, published in Eur Rev Med Pharmacol Sci 2020; 24 (1): 36-42-DOI: 10.26355/eurrev_202001_19893-PMID: 31957816" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19893.

Long noncoding RNA LINP1 promoted proliferation and invasion of ovarian cancer via inhibiting KLF6.

OBJECTIVE: Ovarian cancer is one of the most ordinary fatal cancers. The role of long noncoding ribonucleic acids (lncRNAs) in tumor progression has caught the attention of numerous researchers. In this work, lncRNA LINP1 was studied to identify how it functioned in the progression of ovarian cancer. PATIENTS AND METHODS: Firstly, quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to measure LINP1 expression in ovarian cancer tissues. Furthermore, to identify the function of LINP1 in ovarian cancer, functional experiments were conducted. Also, by performing qRT-PCR and Western blot assay, the underlying mechanism was explored. RESULTS: In this research, LINP1 expression was remarkably higher in ovarian carcinoma samples compared with adjacent tissues. Moreover, cell proliferation, migration, and invasion were inhibited after LINP1 was silenced in the ovarian cancer cells. Besides, the messenger (mRNA) and the protein of KLF6 were overexpressed after LINP1 was silenced. Furthermore, the KLF6 expression level was negatively related to the LINP1 expression level in ovarian cancer samples. CONCLUSIONS: We discovered a potential oncogene in ovarian cancer and identified that LINP1 enhanced cell metastasis and proliferation via down-regulating KLF6.