Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity.

BACKGROUND: Prostate cancer is the second most common cancer in men, and some new target genes are needed to predict the risk of prostate cancer progression and the treatment. METHODS: In this study, the effects of UAP1L1 (UAP1-like-1) on prostate cancer were investigated by detecting the proliferation, migration, invasion and apoptosis of prostate cancer cells in vitro using MTT, wound healing, Transwell and flow cytometry assay, and the tumor growth in vivo. The downstream genes and pathways of UAP1L1 were explored using Ingenuity Pathway Analysis (IPA), and screened by qRT-PCR and western blot. The effects of CDCA8 on prostate cancer cells were also verified in vitro, which was through detecting the change of proliferation, migration, invasion and apoptosis of prostate cancer cells after CDCA8 knockdown. RESULTS: The results indicated that UAP1L1 promoted the proliferation, migration and invasion of prostate cancer cells, which was inhibited by downregulating CDCA8. Furthermore, the promotion of CDCA8 knockdown on cell apoptosis was reduced when UAP1L1 was simultaneously overexpressed. CONCLUSIONS: In conclusion, the results in this study revealed that UAP1L1 promoted the progression of prostate cancer through the downstream gene CDCA8.

Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17.

INTRODUCTION: Accumulating evidence has revealed the critical roles of long noncoding RNAs (lncRNAs) in various cancers. LncRNA SNHG20 has been shown to be a cancer-associated lncRNA in several cancers with diverse mechanisms. However, the clinical references, biological roles, and mechanisms of action of SNHG20 in prostate cancer (PCa) are still unclear. MATERIAL AND METHODS: The expression of SNHG20 in PCa tissues and cell lines was detected by RT-qPCR. The correlations between SNHG20 expression and clinicopathological features were analyzed by χ2 test. The roles of SNHG20 in PCa cell proliferation and migration were detected by CCK-8, EdU incorporation, and transwell assays. The regulatory mechanisms of SNHG20 on DDX17 were detected by dual luciferase reporter assay, RT-qPCR, and western blot. RESULTS: SNHG20 is highly expressed in PCa tissues and cell lines. High expression of SNHG20 is positively correlated with high Gleason score and advanced tumor stage. Functional experiments revealed that overexpression of SNHG20 promotes PCa cell proliferation and migration. SNHG20 knockdown represses PCa cell proliferation and migration. Mechanistically, SNHG20 was verified to act as a competing endogenous RNA (ceRNA) to upregulate DDX17. DDX17 is also highly expressed and has oncogenic roles in PCa. Furthermore, the expression of DDX17 is significantly positively correlated with that of SNHG20 in PCa tissues. Depletion of DDX17 reverses the oncogenic roles of SNHG20 in PCa. CONCLUSIONS: These data showed that SNHG20 promotes PCa cell proliferation and migration via acting as a ceRNA to upregulate DDX17. This study also suggested that SNHG20 may be a potential novel therapeutic target for PCa.

Sum of High-Risk Gene Mutation (SHGM): A Novel Attempt to Assist Differential Diagnosis for Adrenocortical Carcinoma with Benign Adenoma, Based on Detection of Mutations of Nine Target Genes.

There has been no research on applying gene detection to differential diagnosis of adrenocortical carcinoma (ACC). We attempted to explore a novel auxiliary method for differential diagnosis between ACC with benign adrenocortical adenoma (ACA), based on mutations of target genes in tissues. Nine genes were chosen as target genes, including TP53, CTNNB1, ARMC5, PRKAR1A, ZNRF3, RB1, APC, MEN1, and RPL22. Exons sequencing of target genes were performed in 98 cases of tissue samples by FastTarget technology, including 41 ACC tissues, 32 ACA tissues, and 25 normal adrenal gland tissues. Significant mutations were detected and identified, and the clinical information was collected, for further comparative analysis and application to assist differential diagnosis of ACC. We identified 132 significant gene mutations and 227 significant mutation sites in 37 ACC tissues, much more than ACA and normal adrenal gland tissues. Mutation rates of 6 genes in ACC tissues were obviously higher than ACA tissues, including ZNRF3, ARMC5, TP53, APC, RB1, and PRKAR1A, regarded as high-risk genes. The sum of mutated high-risk genes detected in each sample was denominated sum of high-risk gene mutation (SHGM), and the rates of SHGM > 0 and SHGM > 1 in ACC tissues were 73.0% and 62.2%, respectively, both obviously higher than those in ACA tissues, with significant statistic differences. Especially for 8 cases of ACC with diameter < 5 cm, SHGM > 0 and SHGM > 1 were found in 6 samples (75%) and 4 samples (50%), respectively. However, no relevance was found between SHGM and clinical characteristics of ACC. We identified 6 high-risk genes in ACC tissues, with significantly higher mutation rates than ACA or normal adrenal gland tissues. The sum of mutated high-risk genes detected in ACC tissues was denominated SHGM, which was potential to assist the differential diagnosis of ACC with ACA, especially for the small-size ACC.

Ureteral obstruction and hydronephrosis caused by foreign body: A case report and literature review.

RATIONALE: Foreign bodies related ureteral obstruction and hydronephrosis is rare and usually cause numerous problems for clinical physicians. PATIENT CONCERNS: We report a 36-year-old female who was referred to our hospital due to a 4-year history of dull pain on the left back. DIAGNOSIS: X-ray and abdominal CT revealed a foreign body around the upper part of the left ureter with ureteral obstruction and hydronephrosis. INTERVENTIONS: Laparoscopy was performed and a 3-cm sewing needle was removed successfully. OUTCOMES: After 6 months' follow-up, the patient's ureteral obstruction and hydronephrosis were significantly reduced, and the double-J ureteral stent was removed. LESSONS: This case indicated that ureteral obstruction and hydronephrosis caused by foreign bodies needed to be early diagnosed and located. Invasive therapies rather than conservative treatments are preferred to remove the FBs and relieve obstruction.

Open adrenalectomy versus laparoscopic adrenalectomy for adrenocortical carcinoma: a retrospective comparative study on short-term oncologic prognosis.

PURPOSE: Open adrenalectomy (OA) remains the gold standard of surgical therapy for adrenocortical carcinoma, while the role of laparoscopic approach is controversial. We aim to explore the influence of surgical approaches on the oncologic prognosis of adrenocortical carcinoma by comparing the short-term outcomes of patients undergoing OA with those undergoing laparoscopic adrenalectomy (LA). PATIENTS AND METHODS: We retrospectively analyzed the baseline characteristics, perioperative data and short-term prognosis of 42 patients diagnosed with stage I-III adrenocortical carcinoma, receiving OA (n=22) and LA (n=20) as primary therapy. The primary end point was the first recurrence. RESULTS: OA group had larger mean maximum diameter of tumor (10.1±3.6 versus 6.3±2.2 cm) and lesser benefits in operative time, bleeding loss and postoperative hospital stay than laparoscopic group. Mean disease-free survival (DFS) of OA was 44.8±35.1 months, which was longer than 17.5±10.4 months of LA, and the rate of 2-year DFS after primary surgery in the open group was higher than in the laparoscopic group (61.1% versus 21.4%, respectively). Rates of 1- and 3-year DFS showed no significant difference. All patients undergoing LA (11/11) showed local recurrent lesions at the first time of recurrence, while 5 of 13 patients undergoing OA did not show local recurrence (P=0.03). CONCLUSION: OA for adrenocortical carcinoma is superior to laparoscopic approach in terms of DFS and rate of 2-year DFS, in spite of the larger maximum diameter of tumors and lesser benefit during perioperation. After LA, patients are more likely to show local recurrent lesions at the first time of relapse.