Characterization of circSCL38A1 as a novel oncogene in bladder cancer via targeting ILF3/TGF-ß2 signaling axis.

The regulatory role of circRNAs in cancer metastasis has become a focused issue in recent years. To date, however, the discovery of novel functional circRNAs and their regulatory mechanisms via binding with RBPs in bladder cancer (BC) are still lacking. Here, we screened out circSLC38A1 based on our sequencing data and followed validation with clinical tissue samples and cell lines. Functional assays showed that circSLC38A1 promoted BC cell invasion in vitro and lung metastasis of mice in vivo. By conducting RNA pull-down, mass spectrum, and RIP assays, circSLC38A1 was found to interact with Interleukin enhancer-binding factor 3 (ILF3), and stabilize ILF3 protein via modulating the ubiquitination process. By integrating our CUT&Tag-seq and RNA-seq data, TGF-ß2 was identified as the functional target of the circSLC38A1-ILF3 complex. In addition, m6A methylation was enriched in circSLC38A1 and contributed to its upregulation. Clinically, circSLC38A1 was identified in serum exosomes of BC patients and could distinguish BC patients from healthy individuals with a diagnostic accuracy of 0.878. Thus, our study revealed an essential role and clinical significance of circSLC38A1 in BC via activating the transcription of TGF-ß2 in an ILF3-dependent manner, extending the understanding of the importance of circRNA-mediated transcriptional regulation in BC metastasis.

Development and validation of a novel model for predicting the survival of bladder cancer based on ferroptosis-related genes.

The role of ferroptosis, a new form of cell death, in bladder cancer (BC) has not been sufficiently studied. This study aimed to establish a prognostic prediction model for BC patients based on the expression profile of ferroptosis-related genes (FRG). The expression profiles of BC samples with clinical information were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). A total of 80 differentially expressed genes (DEGs) related to FRG were identified among which 37 DEGs were found to have a prognostic value. Eleven genetic markers including SLC2A12, CDO1, JDP2, MAFG, CAPG, RRM2, SLC2A3, SLC3A2, VDAC2, GCH1, and ANGPTL7 were identified through the LASSO regression analysis. The ROC curve analysis showed that the AUC was 0.702, 0.664, and 0.655 for the 1-year, 3-year, and 5-year survival outcomes, respectively. The prediction performance was verified in the TCGA-testing set and external set GSE13507. Multivariate Cox proportional hazards analysis showed that the risk score was an independent prognostic predictor. Moreover, we found differences in gene mutation, gene expression, and immune cell infiltration between the high and low-risk groups of BC patients. Finally, a nomogram was constructed by integrating clinical features and FRG signatures to predict the survival outcomes of BC patients. In addition, the differential expression of FRG mRNA and protein was verified through PCR and HPA online site. The characteristics of 11 FRG genes were examined and a prognostic nomogram for predicting the overall survival of BC was established.

Injectable, Adhesive, and Self-Healing Composite Hydrogels Loaded With Oxybutynin Hydrochloride for the Treatment of Overactive Bladder in Rats.

Object: The aim of this study was to prepare injectable, adhesive, and self-healing composite hydrogels loaded with oxybutynin hydrochloride and verify its function in the treatment of overactive bladder. Method: The ultraviolet (UV) absorption of oxybutynin (Oxy) in the solution was detected using a UV spectrophotometer at 233 nm, and the cumulative drug release was calculated using Origin software. L929 mouse fibroblasts were used to test cell adhesion to OCP50 and OCP100 hydrogels. Both FT-IR and NMR overactive bladder demonstrated that Dex was oxidized to PDA with aldehyde groups. Urodynamic examinations were performed 24 h after intraperitoneal injection in the rat model. The relative expression levels of Orai1 and STIM1 were detected by western blot (WB) and QPCR. Results: After loading Oxy, the shear adhesion under the wet conditions of OCP50 and OCP100 was higher than CP50 and CP100 (p < 0.05), and both were suitable for intravaginal administration. After 72 h of release, oxybutynin released 82.8% in OCP100 hydrogel and 70% in OCP50. Compared to the model, OCP50, CP100, and OCP100 relieved the overactive bladder and inhibited the expression of Orail and STIM1. Conclusions: Oxybutynin hydrogel could provide relief to overactive bladder by decreasing the expression of Orail and STIM1 in rats.

AUP1 regulates lipid metabolism and induces lipid accumulation to accelerate the progression of renal clear cell carcinoma.

Lipid metabolic reprogramming is a prominent feature of clear cell renal cell carcinoma (ccRCC). Lipid accumulation affects cellular energy homeostasis, biofilm synthesis, lipid signal transduction, and phenotypic transformation in ccRCC. Herein, a prognostic-related model was constructed, and the prognostic utility of AUP1, a lipid droplet-regulating very low-density lipoprotein assembly factor, in ccRCC was determined through multiparameter analysis. AUP1 expression was significantly higher in clinical samples than in normal tissues and was closely associated with the clinical stage. The inhibition of AUP1 expression impaired the proliferation, migration, and invasion of ACHN and A498 ccRCC cells in vitro and in vivo. RNA-seq analysis revealed that AUP1 inhibition can significantly reduce the contents of intracellular triglyceride and cholesterol and regulate cell growth by cell cycle arrest, promoting apoptosis and reversing epithelial-mesenchymal transition. AUP1 regulated the synthesis of cholesterol esters and fatty acids (FAs) in ccRCC cells by targeting sterol O-acyltransferase 1 and partially promoted the progression of ccRCC. AUP1 also induced lipid accumulation in ccRCC by promoting the de novo synthesis of FAs (inhibiting protein kinase AMP-activated catalytic subunit alpha 2), inhibiting the rate-limiting enzyme of FA ß oxidation (carnitine palmitoyltransferase 1A), regulating the key enzyme of lipolysis (monoglyceride lipase, MGLL), and inhibiting the lipid transporter StAR-related lipid transfer domain containing 5 (STARD5). However, it did not affect the intracellular cholesterol synthesis pathway. The differential expression and prognostic significance of MGLL and STARD5 in ccRCC should be further studied. AUP1 may serve as a new and effective potential target and prognostic marker for ccRCC.

Immune-Related Genes Are Prognostic Markers for Prostate Cancer Recurrence.

BACKGROUND: Prostate cancer (PCa) is an immune-responsive disease. The current study sought to explore a robust immune-related prognostic gene signature for PCa. METHODS: Data were retrieved from the tumor Genome Atlas (TCGA) database and GSE46602 database for performing the least absolute shrinkage and selection operator (LASSO) cox regression model analysis. Immune related genes (IRGs) data were retrieved from ImmPort database. RESULTS: The weighted gene co-expression network analysis (WGCNA) showed that nine functional modules are correlated with the biochemical recurrence of PCa, including 259 IRGs. Univariate regression analysis and survival analysis identified 35 IRGs correlated with the prognosis of PCa. LASSO Cox regression model analysis was used to construct a risk prognosis model comprising 18 IRGs. Multivariate regression analysis showed that risk score was an independent predictor of the prognosis of PCa. A nomogram comprising a combination of this model and other clinical features showed good prediction accuracy in predicting the prognosis of PCa. Further analysis showed that different risk groups harbored different gene mutations, differential transcriptome expression and different immune infiltration levels. Patients in the high-risk group exhibited more gene mutations compared with those in the low-risk group. Patients in the high-risk groups showed high-frequency mutations in TP53. Immune infiltration analysis showed that M2 macrophages were significantly enriched in the high-risk group implying that it affected prognosis of PCa patients. In addition, immunostimulatory genes were differentially expressed in the high-risk group compared with the low-risk group. BIRC5, as an immune-related gene in the prediction model, was up-regulated in 87.5% of prostate cancer tissues. Knockdown of BIRC5 can inhibit cell proliferation and migration. CONCLUSION: In summary, a risk prognosis model based on IGRs was developed. A nomogram comprising a combination of this model and other clinical features showed good accuracy in predicting the prognosis of PCa. This model provides a basis for personalized treatment of PCa and can help clinicians in making effective treatment decisions.

Prognostic Implications of Immune-Related Gene Pairs Signatures in Bladder Cancer.

Compelling evidence indicates that immune function is correlated with the prognosis of bladder cancer (BC). Here, we aimed to develop a clinically translatable immune-related gene pairs (IRGPs) prognostic signature to estimate the overall survival (OS) of bladder cancer. From the 251 prognostic-related IRGPs, 37 prognostic-related IRGPs were identified using LASSO regression. We identified IRGPs with the potential to be prognostic markers. The established risk scores divided BC patients into high and low risk score groups, and the survival analysis showed that risk score was related to OS in the TCGA-training set (p < 0.001; HR = 7.5 [5.3, 10]). ROC curve analysis showed that the AUC for the 1-year, 3-year, and 5-year follow-up was 0.820, 0.883, and 0.879, respectively. The model was verified in the TCGA-testing set and external dataset GSE13507. Multivariate analysis showed that risk score was an independent prognostic predictor in patients with BC. In addition, significant differences were found in gene mutations, copy number variations, and gene expression levels in patients with BC between the high and low risk score groups. Gene set enrichment analysis showed that, in the high-risk score group, multiple immune-related pathways were inhibited, and multiple mesenchymal phenotype-related pathways were activated. Immune infiltration analysis revealed that immune cells associated with poor prognosis of BC were upregulated in the high-risk score group, whereas immune cells associated with a better prognosis of BC were downregulated in the high-risk score group. Other immunoregulatory genes were also differentially expressed between high and low risk score groups. A 37 IRGPs-based risk score signature is presented in this study. This signature can efficiently classify BC patients into high and low risk score groups. This signature can be exploited to select high-risk BC patients for more targeted treatment.

LncRNA PlncRNA-1 accelerates the progression of prostate cancer by regulating PTEN/Akt axis.

Long non-coding RNAs are key regulators of tumor development and progression, with the potential to be biomarkers of tumors. This study aimed to explore the role of PlncRNA-1 in the progression of prostate cancer (PCa). We found that PlncRNA-1 was up-regulated in 85.29% of PCa tissues and could predict the T stage of PCa patients to a certain extent. Results showed that inhibition of PlncRNA-1 expression potentially promoted cell apoptosis, suppressed the proliferation, migration, and invasion of cells, and triggered G2/M cycle arrest in vitro and in vivo. PlncRNA-1 was mainly localized in the nucleus and PlncRNA-1 expression and phosphatase and tensin homologue (PTEN) expression were negatively correlated. Mechanistically, knockdown of PlncRNA-1 increased expression levels of PTEN protein and phosphorylated PTEN protein, and decreased expression levels of Akt protein and phosphorylated Akt protein. Rescue experiments demonstrated that PTEN inhibitors abolished the changes in PTEN/Akt pathway caused by PlncRNA-1 interference. PlncRNA-1 can promote the occurrence and development of PCa via the PTEN/Akt pathway. PlncRNA-1 may, therefore, be a new candidate target for the treatment of PCa.

Corrigendum to "The SLC Family Are Candidate Diagnostic and Prognostic Biomarkers in Clear Cell Renal Cell Carcinoma".

[This corrects the article DOI: 10.1155/2020/1932948.].

Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis.

Apart from being potential prognostic biomarkers and therapeutic targets, long non-coding RNAs (lncRNAs) modulate the development and progression of multiple cancers. PlncRNA-1 is a newly discovered lncRNA that exhibits the above properties through multiple regulatory pathways. However, the clinical significance and molecular mechanisms of PlncRNA-1 in bladder cancer have not been established. PlncRNA-1 was found to be overexpressed in 71.43% of bladder cancer tissues. Moreover, the expression level correlated with tumor invasion, T stage, age, and number of tumors, but not with gender, recurrent status, preoperative treatment, pathological grade, and tumor size. The expression level of PlncRNA-1 can, to a certain extent, be used as a predictor of the degree of tumor invasion and T stage among BC patients. Inhibiting PlncRNA-1 expression impaired the proliferation, migration, and invasion of T24 and 5637 bladder cancer cells in vitro and in vivo. Specifically, PlncRNA-1 promoter in BC tissues was found to be hypomethylated at position 131 (36157603 on chromosome 21). PlncRNA-1 promoter hypomethylation induces the overexpression of PlncRNA-1. In addition, PlncRNA-1 modulated the expression of smad3 and has-miR-136-5p (miR-136). Conversely, miR-136 regulated the expression of PlncRNA-1 and smad3. PlncRNA-1 mimics competitive endogenous RNA (ceRNA) in its regulation of smad3 expression by binding miR-136. Rescue analysis further revealed that modulation of miR-136 could reverse the expression of smad3 and epithelial-mesenchymal transition (EMT) marker proteins impaired by PlncRNA-1. In summary, PlncRNA-1 has important clinical predictive values and is involved in the post-transcriptional regulation of smad3. The PlncRNA-1/miR-136/smad3 axis provides insights into the regulatory mechanism of BC, thus may serve as a potential therapeutic target and prognostic biomarker for cancer.

The SLC Family Are Candidate Diagnostic and Prognostic Biomarkers in Clear Cell Renal Cell Carcinoma.

Clear cell renal cell carcinoma (ccRCC) is the most common lethal subtype of renal cancer, and changes in tumor metabolism play a key role in its development. Solute carriers (SLCs) are important in the transport of small molecules in humans, and defects in SLC transporters can lead to serious diseases. The expression patterns and prognostic values of SLC family transporters in the development of ccRCC are still unclear. The current study analyzed the expression levels of SLC family members and their correlation with prognosis in ccRCC patients with data from Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), The Cancer Genome Atlas (TCGA), cBioPortal, the Human Protein Atlas (HPA), the International Cancer Genome Consortium (ICGC), and the Gene Expression Omnibus (GEO). We found that the mRNA expression levels of SLC22A6, SLC22A7, SLC22A13, SLC25A4, SLC34A1, and SLC44A4 were significantly lower in ccRCC tissues than in normal tissues and the protein expression levels of SLC22A6, SLC22A7, SLC22A13, and SLC34A1 were also significantly lower. Except for SLC22A7, the expression levels of SLC22A6, SLC22A13, SLC25A4, SLC34A1, and SLC44A4 were correlated with the clinical stage of ccRCC patients. The lower the expression levels of SLC22A6, SLC22A13, SLC25A4, SLC34A1, and SLC44A4 were, the later the clinical stage of ccRCC patients was. Further experiments revealed that the expression levels of SLC22A6, SLC22A7, SLC22A13, SLC25A4, SLC34A1, and SLC44A4 were significantly associated with overall survival (OS) and disease-free survival (DFS) in ccRCC patients. High SLC22A6, SLC22A7, SLC22A13, SLC25A4, SLC34A1, and SLC44A4 expression predicted improved OS and DFS. Finally, GSE53757 and ICGC were used to revalidate the differential expression and clinical prognostic value. This study suggests that SLC22A6, SLC22A7, SLC22A13, SLC25A4, SLC34A1, and SLC44A4 may be potential targets for the clinical diagnosis, prognosis, and treatment of ccRCC patients.

Abdominal cocoon with bilateral cryptorchidism and seminoma in the right testis: a case report and review of literature.

BACKGROUND: Abdominal cocoon is a rare peritoneal lesion and is difficult to diagnose because of its lack of special clinical manifestations. Until now, there is no case report of abdominal cocoon combined with cryptorchidism and seminoma. CASE PRESENTATION: A case of abdominal cocoon with cryptorchidism and seminoma was diagnosed and treated in our hospital. The patient had no symptoms except occasional abdominal pain. He underwent laparoscopy because of bilateral cryptorchidism and seminoma in the right testis. During the surgery, he was diagnosed with abdominal cocoon due to the thick fibrous tissues which was tightly adhered and encased part of intestine like a cocoon. Enterolysis and bilateral cryptochiectomy were performed after the diagnosis and nutritional and symptomatic support was provided after the surgery. The patient recovered well and was discharged soon. The postoperative pathological examination confirmed the presence of bilateral cryptorchidism and seminoma in the patient's right testis. CONCLUSION: There are only a handful of cases where a patient has both abdominal cocoon and cryptorchidism. Since the etiologies of both diseases remain unknown, further research is required to investigate effective diagnosis and treatment for the diseases and explore the potential connection between the two diseases.

Crossed-fused renal ectopia with renal calculi: Two case reports and a review of the literature.

RATIONALE: Crossed renal ectopia (CRE) is a rare congenital anomaly that is frequently associated with gastrointestinal, cardiovascular, genital and bone malformations. To the best of our knowledge, only 35 cases of crossed renal ectopia involving calculi and 30 cases of CRE associated with renal carcinoma have been reported to date. PATIENT CONCERNS: Here, we present 2 cases of crossed renal ectopia. A 59-year-old woman with diabetes presented to our hospital with abdominal pain. The second patient was a 24-year-old woman who complained with abdominal pain with a duration of 1 day. DIAGNOSES: On the basis of abdominal ultrasonography, we suspected a solitary kidney both in the two patients. Combined with retrograde pyelography and 3D computed tomography, case 1 was diagnosed as an S-shaped right-to-left crossed-fused ectopic kidney with many stones in the left (normal) renal pelvis and case 2 was confirmed to have lump right-to-left crossed-fused renal ectopia with two 3-mm stones in the renal pelvis of the 2 kidneys. INTERVENTIONS: Case 1 underwent percutaneous nephrolithotomy while case 2 refused to undergo surgery and underwent conservative treatment for pain relief. OUTCOMES: Two patients have been followed up and have no stones recurrence. LESSONS: Crossed fused renal ectopia is easily misdiagnosed as a solitary kidney. CRE is so rare that the recognition of the disease needs to be improved and effective treatment should be taken timely. According to the two cases and literature review, minimally invasive surgery has become increasingly common to treat CRE with stones and carcinoma.

Correction: Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.

[This corrects the article DOI: 10.18632/oncotarget.15318.].

KMT2D inhibits the growth and metastasis of bladder Cancer cells by maintaining the tumor suppressor genes.

KMT2D, a kind of histone H3 lysine 4 (H3K4) methyltransferase, its abnormal expression confirmed to be associated with diverse tumors, but is lack of defined role in bladder cancer (BC). KMT2D mutation was analyzed using several databases. Immunohistochemistry and clinicopathological analysis of KMT2D in 51 paired of BC tissues and corresponding normal tissues were used to evaluate the relationship between KMT2D and BC. The effects of silencing or over-expressing KMT2D on HTB-9 and T24 cell viability, migration and invasion were performed using MTT, wound scratch and Transwell, respectively. Also, bladder cancer mouse model was established by hypodermic injection of the BC cells. Associated expressions of methylation genes, oncogenes and tumor suppressors were assessed by western blot and quantitative real-time PCR. KMT2D was frequent mutation in various tumors, including BC. It was negative expression in BC tissues and cells, also implicated with tumor stages and lymph node metastasis. In silencing KMT2D HTB-9 and T24 cells, cell viability, migration and invasion were notably promoted. Meanwhile, knockdown of KMT2D benefited to solid tumor formation in vivo. However, over-expressing KMT2D represented contrary results. Especially, KMT2D over-expression induced the activity of H3K4 monomethylation (me1), and effectively enhanced PTEN and p53 expressions as well as repressed STAG2 expression. Meanwhile, KMT2D had no obvious effect on Survivin. This work suggested an anti-tumor role for KMT2D in vitro and in vivo, as well as provided a possible tumor inhibition mechanism in which KMT2D enhanced H3K4me1 activity to support the expressions of tumor suppressors.

HUWE1 upregulation has tumor suppressive effect in human prostate cancer cell lines through c-Myc.

PURPOSE: We investigated the regulatory function of HECT, UBA and WWE domain-containing protein 1, E3 ubiquitin protein ligase (HUWE1) in human prostate cancer (CaP). METHODS: HUWE1 was overexpressed (through transfection) or downregulated (through lentiviral transduction) in CaP cell lines, PC3 and DU145 cells. The functions of HUWE1 overexpression or downregulation on CaP cancer cell proliferation, migrationin vitro, and explant in vivo were examined. In addition, the regulatory effect of HUWE1 on c-Myc expression was assessed. In HUWE1-overexpressed CaP cells, c-Myc was further upregulated to assess whether c-Myc was directly involved in HUWE1-induced regulation in CaP. RESULTS: HUWE1 overexpression inhibited CaP proliferation and migrationin vitro, and explant growth in vivo. On the other hand, HUWE1 downregulation had no effects on CaP in vitro. C-Myc was downregulated in HUWE1-overexpressed, but un-changed in HUWE1-downregulated, CaP cells. Further upregulating c-Myc in HUWE1-overexpressed CaP cells reversed the tumor-suppressing effects by HUWE1-overexpression on cancer proliferation and migration in vitro. CONCLUSION: HUWE1 overexpression could functionally suppress CaP development bothin vitro and in vivo, possibly by inverse regulation on c-Myc.

Utility of fluorescence in situ hybridization analysis for detecting upper urinary tract-urothelial carcinoma.

OBJECTIVES: The objective of this study was to evaluate the clinical utility of fluorescence in situ hybridization (FISH) in the detection of upper urinary tract-urothelial carcinoma (UUT-UC). METHODS: Between November 2011 and November 2015, voided urine specimens from 52 consecutive patients with UUT-UC and 26 controls were collected for both FISH test and cytology. Sensitivity and specificity of FISH test and cytology were determined and compared. The frequency of chromosomal aberrations was also analyzed. RESULTS: For FISH analysis, the sensitivity was 79.5% and specificity was 96.3%. For cytology, the sensitivity was 27.3% and specificity was 100%. The overall sensitivity for FISH was significantly higher than that of in single value-based urine cytology (79.5% vs. 27.3%, respectively, P < 0.001). The sensitivities of FISH and cytology by grade were 64.3% vs. 28.6% for low-grade urothelial carcinomas (P = 0.128) and 86.7% vs. 26.7% for high-grade urothelial carcinomas (P < 0.001), respectively. Twenty-seven (77.1%) cases were positive due to the gain of two or more chromosomes in five or more urinary cells, among which, 21 (60%) cases showed positivity in all the 4 chromosomes, 7 (20%) cases matched the criterion that 10 or more cells gained a single chromosome, whereas only 1 (2.9%) case was positive because of the homozygous deletion of 9p21 in 12 or more cells. CONCLUSIONS: FISH has superior sensitivity and similar specificity in the detection of UUT-UC, compared with cytology. The present findings indicated that FISH can be applied as a noninvasive diagnostic tool for suspected UUT-UC patients.

Upregulation of long non-coding RNA PlncRNA-1 promotes proliferation and induces epithelial-mesenchymal transition in prostate cancer.

OBJECTIVE: To confirm that PlncRNA-1 regulates the cell cycle in prostate cancer cells and induces epithelial-mesenchymal transition (EMT) in prostate cancer through the TGF-ß1 pathway. RESULTS: PlncRNA-1 and TGF-ß1 expression levels were significantly higher in prostate cancer tissues than in normal prostate tissues (P < 0.05) and were significantly positively correlated. TGF-ß1, N-cadherin and Cyclin-D1 were downregulated and E-Cadherin was upregulated in LNCAP cells after silencing of PlncRNA-1, as determined by real-time PCR and Western blot. TGF-ß1, N-cadherin and Cyclin-D1 were upregulated and E-cadherin was downregulated in C4-2 cells, as determined by real-time PCR and Western blot. Overexpression of PlncRNA-1 in C4-2 cells was observed when TGF-ß1 inhibitor LY2109761 was added. Western blot analysis showed that compared with their expression when TGF-ß1 inhibitor LY2109761 was not added, N-Cadherin and CyclinD1 expression decreased and E-Cadherin expression increased. Transwell results showed that the invasive ability of C4-2 cells was enhanced after overexpression of PlncRNA-1, and the invasion ability was decreased after addition of TGF-ß1 inhibitor LY2109761. The cell cycle was blocked by overexpression of PlncRNA-1 in C4-2 and by the addition of TGF-ß1 inhibitor LY2109761, as determined by flow cytometry. In vitro experiments showed that PlncRNA-1 can regulate the growth of prostate cancer cells and EMT through the TGF-ß1 pathway. In vivo experiments also confirmed the above results. Tumor growth was significantly blocked by overexpressing PlncRNA-1 in C4-2 cells and by the TGF-ß1 inhibitor LY2109761 in animal experiments. MATERIALS AND METHODS: The expression levels of PlncRNA-1 and TGF-ß1 were analyzed in 19 prostate cancer tissue samples and in adjacent normal tissue samples, 4 Pca cell lines, including LNCaP, C4-2,DU145, and PC3, and 1 normal prostate epithelial cell line RWPE-1. LNCAP cells were divided into the LNCAP control group and the LNCAP-PlncRNA-1-siRNA group. Cells from the prostate cancer cell line C4-2 were divided into the C4-2 control group and the C4-2-PlncRNA-1 experimental group. Changes in TGF-ß1, E-cadherin and N-cadherin were detected by qPCR and Western Blot assay after silencing and overexpression of PlncRNA-1. The cell cycle, cell invasion, and levels of Cyclin-D1, E-Cadherin, and N-Cadherin were observed after adding TGF-ß1 inhibitor LY2109761 in the C4-2-PlncRNA-1 group. The effects of TGF-ß1 inhibitor LY2109761 on the tumorigenicity of C4-2 cells after overexpression of PlncRNA-1 was investigated in vivo. CONCLUSIONS: PlncRNA-1 is an oncogene that regulates the cell cycle, cyclin-D1 and EMT in prostate cancer cells through the TGF-ß1 pathway.

Calcifying Fibrous Tumor of the Tunica Vaginalis Testis: A Report of 2 Cases.

OBJECTIVE: To improve the clinical diagnosis and treatment of calcifying fibrous tumor (CFT) of the tunica vaginalis testis, we discussed clinical manifestations and pathologic features of CFT. MATERIALS AND METHODS: A retrospective analysis of 2 cases of CFT that occurred in our hospital was performed, and we also reviewed the literature and research reports. RESULTS: Both patients underwent local excision with testis preservation surgery, and pathology examination confirmed the presence of multiple CFTs of the tunica vaginalis testis. CONCLUSION: CFTs are rare, benign multiple lesions, and the recognition of which needs to be improved to avoid overtreatment. We are the first to describe 2 cases of CFT combined with hepatitis B, but additional studies are needed to confirm the relationship between these conditions.

PlncRNA-1 induces apoptosis through the Her-2 pathway in prostate cancer cells.

To determine whether PlncRNA-1 induces apoptosis in prostate cancer cells through the Her-2 pathway. The expression of PlncRNA-1, Her-2, and related cyclin proteins in 23 cases of prostate cancer and adjacent normal tissues was analyzed and compared. LNCaP cells were divided into a control group and an LNCaP-PlncRNA-1-siRNA experimental group. Normal prostate RWPE-1 cells were divided into an RWPE-1 control group and an RWPE-1-PlncRNA-1 experimental group. After PlncRNA-1 silencing and overexpression, changes in Her-2 and cyclinD1 expression levels were detected both in vivo and in vitro. In prostate cancer tissues, Her-2 and PlncRNA-1 were highly expressed and significantly correlated. In LNCaP cells, the expression of Her-2 and cyclinD1 decreased following the downregulation of PlncRNA-1 as assessed by real-time PCR and Western blotting. In RWPE-1 cells, the expression of Her-2 and cyclinD1 increased following PlncRNA-1 overexpression. Flow cytometry revealed that the proportion of LNCaP cells in G2/M phase was significantly increased after PlncRNA-1 silencing and that the proportion of RWPE-1 cells in G2/M phase was significantly decreased after PlncRNA-1 overexpression. Furthermore, animal experiments validated these results. In conclusion, in prostate cancer, PlncRNA-1 regulates the cell cycle and cyclinD1 levels and can also regulate proliferation and apoptosis in prostate cancer cells through the Her-2 pathway.