Intravenous leiomyomatosis (IVL) is a rare benign tumor. The study aimed to assess outcomes of patients treated surgically for IVL.Between November 2002 and January 2015, 76 patients were treated for IVL. The stage of IVL was evaluated preoperatively by echocardiography and enhanced computerized tomography (CT) scan, and graded into 4 stages according to intravascular tumor progression. We recorded age, lower limb edema before surgery, surgical parameters, and hospitalization expenses. Patients were followed up every 6 months and tumor recurrence was assessed by CT and ultrasound. Patients were followed up for a mean of 4.5 ± 2.5 years (range 1–13 years) and there was no operative, hospital, or long-term mortality or were lost to follow-up.The rate of lower extremity edema, amount of blood loss, postoperative transfusion, length of intensive care unit (ICU) stay, postoperative hospitalization, and hospitalization expenses differed significantly between patients at different presurgery stages. Tumors recurred in 4 of 7 patients with stage I IVL that opted for surgery that preserved the ovaries and uterus. No recurrence was observed in patients graded stage II or more, in all of which the uterus and ovaries were removed. Recurrence was observed in only 4 of 76 cases of IVL, all of whom opted for surgery that spared the ovaries and uterus.Different surgical strategies should be decided based on the staging to completely remove the tumor and ensure the safety of patients. Removal of both ovaries is necessary for inhibiting tumor growth and avoiding recurrence.

PAAs must be seriously classified by aetiology to be treated appropriately. Patients with giant-size PAAs, and those with pulmonary hypertension, anatomical anomalies, and rapid growth and compression of neighbouring critical structures, are proper candidates for surgery. Surgical options include aneurysm repair and replacement with allogeneic/synthetic grafts, depending on the situation. Additionally, the correction of associated abnormalities should be performed simultaneously during surgery. Surgical outcomes are effective, and long-term prognoses are satisfactory.

MicroRNAs (miRNAs) have emerged as important regulators in cancer that are implicated in regulation of various cellular processes. miR-382 has been proposed as a tumor suppressor by several recent studies. However, the function of miR-382 in prostate cancer remains unknown. In this study, we aimed to investigate the potential function of miR-382 in prostate cancer. We found that miR-382 was significantly decreased in prostate cancer specimens and cancer cell lines. The overexpression of miR-382 in prostate cancer cells markedly inhibited cell proliferation, migration, and invasion. In contrast, miR-382 suppression exhibited an opposite effect. Target analysis predicted that chicken ovalbumin upstream promoter transcription factor II (COUP‑TFII) was a direct target of miR-382. This prediction was experimentally confirmed by dual-luciferase reporter assay, real-time quantitative polymerase chain reaction, and western blot analysis. Our results further demonstrated that miR-382 inhibited the downstream genes of COUP‑TFII, including Snail and matrix metalloproteinase 2 (MMP2). Moreover, the restoration of COUP‑TFII expression significantly blocked the inhibitory effect of miR-382 on cell proliferation, migration, and invasion, and Snail expression. Taken together, this study suggests that miR-382 inhibits prostate cancer cell proliferation and metastasis through inhibiting COUP‑TFII, representing an important new mechanism for understanding prostate cancer pathogenesis and providing a novel therapeutic candidate target for prostate cancer therapy.

Calcific aortic valve disease (CAVD) is the most common heart valve disorder, yet its mechanism remains poorly understood. Valve interstitial cells (VICs) are the prevalent cells in aortic valve and their osteogenic differentiation may be responsible for calcific nodule formation in CAVD pathogenesis. Emerging evidence shows microRNA (miRNA, or miR) can function as important regulators of many pathological processes, including osteogenic differentiation. Here, we aimed to explore the function of miR-449c-5p in CAVD pathogenesis. In this study, we demonstrated the role of miR-449c-5p in VICs osteogenesis. MiRNA microarray assay and qRT-PCR results revealed miR-449c-5p was significantly down-regulated in calcified aortic valves compared with non-calcified valves. MiR-449c-5p overexpression inhibited VICs osteogenic differentiation in vitro, whereas down-regulation of miR-449c-5p enhanced the process. Target prediction analysis and dual-luciferase reporter assay confirmed Smad4 was a direct target of miR-449c-5p. Furthermore, knockdown of Smad4 inhibited VICs osteogenic differentiation, similar to the effect observed in up-regulation miR-449c-5p. In addition, animal experiments proved indirectly miR-449c-5p could alleviate aortic valve calcification. Our data suggested miR-449c-5p could function as a new inhibitory regulator of VICs osteogenic differentiation, which may act by targeting Smad4. MiR-449c-5p may be a potential therapeutic target for CAVD.