Hydrogen (H2) has advantages that lead it to be used as a novel antioxidant in preventive and therapeutic applications. H2 can permeate into biomembranes, cytosol, mitochondria and nuclei, and can be dissolved in water or saline to produce H2 water or H2‑rich saline. H2 selectively reduces oxidants of the detrimental reactive oxygen species (ROS), including hydroxyl radicals (·OH) and peroxynitrite (ONOO‑), which serve a causative role in the promotion of tumor cell proliferation, invasion and metastasis, but do not disturb metabolic oxidation‑reduction reactions in cell signaling. Compared with traditional antioxidants, H2 is a small molecule that can easily dissipate throughout the body and cells; thus, it may be a safe and effective antioxidant for inflammatory diseases and cancer, since ROS usually initiates tumor progression. Treatment with H2 may involve correction of the oxidative/anti‑oxidative imbalance and suppression of inflammatory mediators. Therefore the present review will discuss the anti‑inflammatory and anti‑tumorigenic action of H2 via ROS.

To elucidate the mechanisms of nuclear estrogen receptor (ER)-mediated and G protein-coupled receptor 30 (GPR30)-mediated signaling in the regulation of proliferation in ER-positive and ER-negative endometrial cancer cells, two human endometrial carcinoma cell lines, Ishikawa (ER-positive) and KLE (ER-negative), were used. PCR and Western blot analyses were used to determine the effects of estrogen stimulation on the activation of Notch and GPR30-PI3K/AKT signaling. Cell growth was investigated using MTT assays. Overexpression of ER in ER-negative cells was achieved by plasmid transfection and was used to investigate the effects on cellular growth and Notch signaling. GPR30-mediated signaling was evaluated using siRNA interference. Estrogen stimulated cell proliferation in both cell lines, it activated Notch signaling in ER-positive Ishikawa cells, but not in ER-negative KLE cells. Blockade of this signaling by a Notch inhibitor resulted in partial arrest of estrogen-induced cell proliferation in Ishikawa cells. Overexpression of ER in KLE cells restored estrogen-enhanced Notch signaling and further promoted cell growth. GPR30, as a new G-protein-coupled estrogen receptor, was detected in both cell lines, but was stronger in ER-negative KLE cells. Depletion of GPR30 in KLE cells abolished estrogen-induced PI3K/AKT signaling activation and resulted in inhibition of cell proliferation. Conclusively, regulation of proliferation in nuclear ER-positive endometrial cancer cells is mediated by both ER-Notch signaling and GPR30-PI3K/AKT signaling, whereas only the latter pathway is involved in the regulation of growth in nuclear ER-negative endometrial cancer cells.

The aberrant expression of miR107‑5p is closely related to the development of several types of human cancers. However, the role of miR‑107‑5p in endometrial carcinoma (EC) has not been fully confirmed. In the present study, we aimed to explore the function of miR‑107‑5p in EC carcinogenesis. EC samples and normal endometrial tissues were obtained by laser capture microdissection. It was determined that the expression of miR‑107‑5p in EC was significantly higher than that in normal endometrium, and higher miR‑107‑5p expression was related to advanced FIGO stages, lymph node metastasis and myometrial invasion in EC patients. Blocking miR‑107‑5p significantly inhibited cell proliferation, migration and invasion of EC cells in vitro and in vivo. The results of bioinformatic algorithms and luciferase reporter assays revealed that estrogen receptor α (ERα) was a direct target of miR‑107‑5p. miR‑107‑5p downregulated the expression of ERα mRNA and protein. In conclusion, our results highlighted that miR‑107‑5p is a novel prognostic factor that targets ERα to promote tumor proliferation and invasion of EC.

This research was carried out to investigate the effectiveness, rationality, and safety of laparotomy management compared with uterine artery embolization (UAE) combined with methotrexate (MTX) for the treatment of deep implantation cesarean scar pregnancy (CSP II). Data from 29 patients seen between June 2008 and February 2012 were retrospectively analyzed. The patients were divided into the surgery group and the UAE combined with MTX group according to the treatment they received. We compared the clinical characteristics and treatment outcomes between the two groups. The patients' clinical characteristics did not differ between the surgery group and the UAE combined with MTX group. However, the mean blood loss was decreased in the surgery group compared with the UAE combined with MTX group (90 ± 4.5 mL vs. 286 ± 5.2 mL, p < 0.05). No patients required blood transfusion in the surgery group, whereas two patients in the UAE combined with MTX group received blood transfusions. The length of time for the serum beta human chorionic gonadotropin (β-HCG) level to normalize, the time required for the disappearance of the gestational mass, and the duration of hospital stay were significantly less in the surgery group than in the UAE combined with MTX group (13.7 ± 1.0 days vs. 40.7 ± 1.7 days, 7.1 ± 1.3 days vs. 135.4 ± 6.7 days, and 11.0 ± 1.2 days vs. 41.4 ± 3.2 days, respectively; p < 0.01). Although the treatment success rate did not differ significantly between the two groups, the success rate was 100% for the surgery group and 73% for the UAE combined with MTX group. Surgical treatment can remove gestational masses and allow wound repair. Moreover, laparotomy is available in almost all hospitals. Thus, surgery can be an effective and reasonable treatment for CSP II.

Background: We demonstrated that drinking hydrogen-rich water (HRW) inhibits endometrial tumor growth in our previous work. This research is to identify differentially expressed proteins (DEPs) between HRW and purified water groups in a xenograft mouse model of endometrial cancer (EC). Methods: Samples were analyzed using tandem mass tags (TMTs) coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS). DEPs were identified using bioinformatics to determine potential molecular functions and immunohistochemical (IHC) staining. Results: In total, 11 DEPs were identified in the HRW group relative to the control. The up-regulated proteins included Gatad1, Ttyh3, Nek4, Dyrk2, and Gimap1, while the down-regulated proteins included SP1, Msl1, Plekha7, Dtwd2, MSRA, and KRAS. Gene Ontology (GO) annotations and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were associated with the binding region, biological regulation, endocrine resistance, estrogen signaling, choline metabolism in cancer and human cytomegalovirus infection. Furthermore, network analysis indicated that KRAS and MSRA interact with YWHAE. KRAS, YWHAE and SP1 were strongly expressed, while MSRA was weak expressed in atypical hyperplasia and EC tissue as well as in HRW group in xenograft tumor tissue. Conclusions: KRAS, YWHAE, SP1 and MSRA might be regarded as focused biomarkers to assess the prognosis of EC.

Ovarian cancer (OC) is one of five leading causes of cancer related death among women worldwide. Although treatment has been improving, the survival rate has barely improved over the past 30 years. The fatality rate is due to asymptomatic early signs and the lack of long-term effective treatment strategies for advanced disease. Angiogenesis is an important process in tumour growth and metastasis and is the creation of new blood vessels from existing blood vessels. It is a dynamic and complex process involving various molecular regulatory pathways and multiple mechanisms. The inhibition of angiogenesis has become a recognized therapeutic strategy for many solid tumours. While benefits in progression-free survival have been observed, the OS is far from satisfactory for OC patients who receive antiangiogenic therapy. In this article, the present research status of angiogenesis in OC was reviewed and the reasons for poor antiangiogenic therapeutic effects was explored with the aim to identify potential therapeutic targets that may improve the effect of antiangiogenic therapies.