Retraction of "miR-223-3p alleviates TGF-ß-induced epithelial-mesenchymal transition and extracellular matrix deposition by targeting SP3 in endometrial epithelial cells".

[This retracts the article DOI: 10.1515/med-2022-0424.].

MiR-4284 inhibits sensitivity to paclitaxel in human ovarian carcinoma SKOV3ip1 and HeyA8 cells by targeting DMC1.

An increasing number of studies have confirmed that microRNAs (miRNAs) are involved in various biological processes, including tumor growth and drug resistance. MiR-4284 has been proved to be abnormally regulated in several cancers, but the function of miR-4284 in ovarian carcinoma (OC) is unclear. Paclitaxel resistance is a key obstacle in OC treatment. Here, the role of miR-4284 in cell sensitivity to paclitaxel in OC was investigated. Two OC cell lines (SKOV3ip1 and HeyA8) were utilized for the establishment of paclitaxel-resistant cell lines. Reverse transcription-quantitative PCR (RT-qPCR) was applied to analyze the levels of miR-4284 and potential mRNAs in OC cell lines. Western blotting was performed to evaluate the levels of DNA meiotic recombinase 1 (DMC1) protein and cell cycle-associated proteins. Identification of the relationship between miR-4284 and DMC1 was achieved by luciferase reporter assay. CCK-8 and flow cytometry assays were utilized for evaluating the impact of miR-4284 on the malignant characteristics of paclitaxel-resistant OC cells. MiR-4284 was upregulated in paclitaxel-resistant OC cell lines and correlated with an adverse prognosis in OC patients. Depletion of miR-4284 suppressed cell proliferation and cell cycle progression of paclitaxel-resistant OC. MiR-4284 targeted DMC1 which was downregulated in paclitaxel-resistant cells and reversed the inhibitory influence of miR-4284 silencing on the malignant characters of paclitaxel-resistant OC cells. MiR-4284 targets DMC1 to suppress sensitivity to paclitaxel in human OC cells.

miR-223-3p alleviates TGF-ß-induced epithelial-mesenchymal transition and extracellular matrix deposition by targeting SP3 in endometrial epithelial cells.

Intrauterine adhesion (IUA) is the clinical manifestation of endometrial fibrosis. The dysregulation of microRNAs (miRNAs) has been confirmed to implicate in a diversity of human diseases, including IUA. Nevertheless, the specific function of miR-223-3p in IUA remains to be clarified. Reverse transcription quantitative polymerase chain reaction analysis displayed the downregulation of miR-223-3p in IUA tissues and endometrial epithelial cells (EECs). Results from wound healing assay, Transwell assay and western blotting showed that TGF-ß facilitated the migration and invasion of EECs and induced epithelial-mesenchymal transition (EMT) process as well as extracellular matrix (ECM) deposition. Overexpression of miR-223-3p in EECs was shown to suppress the effects induced by TGF-ß. Bioinformatics analysis and luciferase reporter assay revealed the binding relation between miR-223-3p and SP3. SP3 was highly expressed in IUA and its expression was inversely correlated with miR-223-3p expression in IUA tissue samples. Additionally, upregulation of SP3 reversed the influence of miR-223-3p on the phenotypes of EECs. In conclusion, miR-223-3p alleviates TGF-ß-induced cell migration, invasion, EMT process and ECM deposition in EECs by targeting SP3.

MiR-455-5p upregulation in umbilical cord mesenchymal stem cells attenuates endometrial injury and promotes repair of damaged endometrium via Janus kinase/signal transducer and activator of transcription 3 signaling.

Umbilical cord mesenchymal stem cells (UCMSCs) are regarded as an ideal source for clinical use. Increasing evidence has suggested that microRNAs (miRNAs) work as a crucial regulator in the development of plentiful diseases, including intrauterine adhesions (IUA). Herein, we investigated the specific impacts of UCMSCs overexpressing miR-455-5p in IUA. UCMSCs were cocultured with endometrial stromal cells (ESCs). Thirty-two female mice were divided into four different treated groups: sham, model, model + UCMSC-miR-NC and model + UCMSC-miR-455-5p. Mice in model groups were induced by uterine curettage. MiR-455-5p overexpressed UCMSCs facilitated the proliferation and cell cycle progression of ESCs according to 5-ethynyl-2'-deoxyuridine assay and flow cytometry analysis. Hematoxylin-eosin and Masson staining revealed that miR-455-5p upregulation in UCMSCs increased the number of endometrial glands and suppressed endometrial fibrosis in murine uterine tissues. Western blotting displayed that miR-455-5p overexpressed UCMSCs promoted the activation of Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling in ESCs and murine uterine tissues. Mechanistically, miR-455-5p targeted 3' untranslated region of suppressor of cytokine signaling 3 (SOCS3), which was confirmed by luciferase reporter assay. Reverse transcription quantitative polymerase chain reaction demonstrated that miR-455-5p was lowly expressed and SOCS3 was highly expressed in murine uterine tissues of IUA model. Moreover, Pearson correlation analysis showed that their expression was inversely correlated. Rescue assays suggested that inhibiting JAK/STAT3 signaling reversed effects of miR-455-5p on the behaviors of ESCs. The results indicated that miR-455-5p overexpression in UCMSCs helps to attenuate endometrial injury and repair damaged endometrium by activating SOCS3-mediated JAK/STAT3 signaling.

Use of biogas fluid-soaked water hyacinth for cultivating Pleurotus geesteranus.

Experiments were carried out to test the viability of growing Pleurotus geesteranus on media containing varying amounts of crushed water hyacinth slices, which were soaked in pig farm biogas fluid and dried. The water hyacinth material was utilized to substitute sawdust in the media for mushroom cultivation. Mushroom fruiting bodies harvested were evaluated for yield, amino acid and heavy metal contents. Among the eight treatment groups, the greatest yield and highest amino acid content in the mushrooms were obtained when the proportions of water hyacinth and sawdust in the medium were equal. The concentrations of heavy metals, Hg, Pb and Cd, in most of the present mushroom samples did not exceed the maximum allowed levels according to the limits set forth by the food hygienic and safety regulations for edible mushrooms in China. The proposed waste utilization of water hyacinth could conceivably benefit the environment in various aspects including conservation of forest by reducing the demand on natural woods for mushroom production.

[Effect of exogenous zinc addition on cell protective enzyme activities in the fruit bodies of Lentinus giganteus].

OBJECTIVE: The effects of exogenous Zn addition on cell protective enzyme activities in the fruit bodies of Lentinus giganteus were studied. METHODS: ZnSO4 was used as exogenous Zn and added into culture medium. The final Zn concentrations in culture media were 0, 10, 20, 30, 40, 50 mg/kg respectively. The activities of superoxide dismutase (SOD), peroxidase (POD), polyphenol oxidase (PPO), malondialchehyche (MDA) content and soluble protein content in the fruit bodies were analyzed by spectrophotometry; catalase (CAT) was determined by potassium permanganate titration. RESULTS: The content of soluble protein and SOD, POD and CAT activities in the fruit bodies of L. giganteus were significantly increased (P < 0.01), but PPO activity (P < 0.01) and MDA content (P < 0.05) was significantly decreased in the treatment of 30 mg/kg Zn concentration. The content of soluble protein and SOD, POD and CAT activities showed a decreasing trend with the increase of Zn concentration, but MDA content was significantly increased (P < 0.01 and P < 0.05). CONCLUSION: High Zn concentration caused the increase of MDA contents and the decrease of SOD, POD and CAT activities in the fruit body of L. giganteus. It will destroy the protective enzyme system, cause the accumulation of free radicals and thus intensify membrane lipid peroxidation. Appropriate Zn concentration improved the protective enzyme activities, and lightened the harm of membrane from lipid peroxidation.