Background The Wilms’ tumor suppressor WT1 is reported to work in a range of physiological processes at both transcriptional and posttranscriptional level. WT1-associating protein (WTAP), a nuclear protein co-localized with splicing factors, also plays a vital role in cellular function and cancer progression. However, little is known about the role of WTAP in ovarian cancer and the underlying mechanism. Materials and methods To evaluate the expression of WTAP, multiple means were applied in clinical tissues, including immunohistochemistry, quantitative reverse transcriptase PCR (qRT-PCR), and Western blot. Two representative ovarian cancer cell lines (3AO and SKOV3) were used to assess the malignant influence of WTAP on proliferation, apoptosis, and migration. To explore its function, WTAP was additionally down-regulated by lentivirus. Results High expression of WTAP in high-grade serous ovarian carcinoma (HGSOC) predicted a shorter overall survival ( P <0.01). Furthermore, WTAP expression was higher in HGSOC, compared with that in normal ovary group ( P <0.01), benign ovarian tumor group ( P <0.01), and non-HGSOC group ( P <0.05). In HGSOC, high expression of WTAP was significantly related with the lymph node metastasis ( P <0.05). In ovarian cancer cell lines, cell proliferation and migration were considerably reduced after WTAP was down-regulated, while apoptotic rate was increased. Moreover, the effect of WTAP in 3AO and SKOV3 might be relevant with MAPK and AKT signaling pathways. Conclusion WTAP is highly expressed in HGSOC, and indicates a worse survival outcome. Therefore, it is highly possible that WTAP has a prognostic implication in the patients of HGSOC. In addition, WTAP down-regulation also plays a tumor suppressor role in 3AO and SKOV3 cell lines.

Cancer is expected to rank as the leading cause of death worldwide due to increasing morbidity and mortality. Long noncoding RNAs (lncRNAs) have been found to play pivotal roles in multiple biological processes, such as transcriptional interference, posttranscriptional regulation and epigenetic modification. Small nucleolar RNA host gene 15 (SNHG15), a snoRNA host gene which produces a short half-lived lncRNA, was reported to be upregulated in tumor cells and participate in the occurrence and development of multiple cancers. And more than half of the SNHG15 research in cancers has been published within the last 2 years. In this review, we summarized the current evidence concerning the biological functions and molecular mechanisms of SNHG15 in various cancers, including gastric, hepatocellular, pancreatic, colorectal, breast, and thyroid cancer, osteosarcoma, glioma, lung cancer, renal cell carcinoma, and epithelial ovarian cancer. SNHG15 plays critical roles in regulation of cell proliferation, migration and invasion of tumors via different potential mechanisms. Moreover, the abnormal expression of SNHG15 was associated with clinical features of patients with cancers. Consequently, SNHG15 could be considered as a promising biomarker for cancer diagnosis, prognosis or treatment.

Purpose Ovarian cancer is the leading cause of death in gynecologic malignancies. Growing evidences demonstrate that a complicated relationship exists between the gut microbiota and cancer treatment. However, there are few studies explored the alterations of gut microbiota in ovarian cancer patients following anti-cancer treatments. Therefore, we aim to analyze the changes of the gut microbiota in ovarian cancer patients treated with radical surgery and chemotherapy. Patients and Methods The microbial genes were examined from a total of 75 fecal samples from 18 ovarian cancer patients, including 10 preoperative fecal samples (Group B), 4 postoperative fecal samples (Group M0), as well as 61 fecal samples after first to fifth cycles of chemotherapy, using 16S rRNA sequencing. Results Our results showed that fecal samples collected in postoperative (Group M0) exhibited significant decreases in abundance of Bacteroidetes and Firmicutes, while a significant increase in abundance of Proteobacteria compared with preoperative (Group B) fecal samples. LEfSe analysis identified that Bilophila and Faecalibacterium are the key genera in Group B, while Klebsiella and Enterococcus are the key genus in Group M0. Compared with before chemotherapy, the abundance of Bacteroidetes and Firmicutes increased, and the abundance of Proteobacteria decreased after chemotherapy. In addition, anaerobic bacteria, such as Bacteroides, Collinsella and Blautia , exhibited significant increases after chemotherapy. Moreover, we observed that certain bacterial genera were significantly correlated with clinicopathological characteristics of ovarian cancer patients. Conclusion Our study suggested that radical surgery and chemotherapy altered the composition of gut microbiota in ovarian cancer patients. Therapeutic strategies targeting the gut microbiota may be beneficial for the clinical treatment of ovarian cancer.