A single-nucleotide polymorphism in PvPW1 encoding ß-1,3-glucanase 9 is associated with pod width in Phaseolus vulgaris L.

Pod width influences pod size, shape, yield, and consumer preference in snap beans (Phaseolus vulgaris L.). In this study, we map PvPW1, a quantitative trait locus associated with pod width in snap beans, through genotyping and phenotyping of recombinant plants. We identify Phvul.006G072800, encoding the ß-1,3-glucanase 9 protein, as the causal gene for PvPW1. The PvPW1G3555 allele is found to positively regulate pod width, as revealed by an association analysis between pod width phenotype and the PvPW1G3555C genotype across 17 bi-parental F2 populations. 97.7% of the 133 wide pod accessions carry PvPW1G3555, while 82.1% of the 78 narrow pod accessions carry PvPW1C3555, indicating strong selection pressure on PvPW1 during common bean breeding. Re-sequencing data from 59 common bean cultivars identify an 8-bp deletion in the intron linked to PvPW1C3555, leading to the development of the InDel marker of PvM436. Genotyping 317 common bean accessions with PvM436 demonstrated that accessions with PvM436247 and PvM436227 alleles have wider pods compared to those with PvM436219 allele, establishing PvM436 as a reliable marker for molecular breeding in snap beans. These findings highlight PvPW1 as a critical gene regulating pod width and underscore the utility of PvM436 in marker-assisted selection for snap bean breeding.

MiR-223-3p targets FOXO3a to inhibit radiosensitivity in prostate cancer by activating glycolysis.

AIMS: The incidence and detection rate of prostate cancer in China have been increasing in recent years. Radiotherapy is the ideal treatment for non-metastatic prostate cancer (PCa), but the effectiveness of radiotherapy is greatly discounted due to radio resistance. Therefore, relieving the radiotherapy resistance of PCa is key to improve the clinical efficacy of PCA. MAIN METHODS: Cell proliferation was estimated using the MTT and clone formation assays. Cell apoptosis was estimated using the Annexin V-FITC/propidium iodide (PI) staining assay. Glucose uptake and lactose and ATP production were used to detect glycolysis. KEY FINDINGS: miR-223-3p was significantly upregulated in clinically collected urine samples and PCa cells with low radiosensitivity. Enhancing miR-223-3p reduced radiosensitivity further, while inhibiting miR-223-3p improved the radiosensitivity of PC3 and LNCaP cells. Importantly, miR-223-3p regulated radiosensitivity by enhancing cell glycolysis. FOXO3a was a key target of miRNA-223-3p regulating glycolysis and radiosensitivity. Overexpression of FOXO3a abated the glycolysis level and alleviated the radioresistance caused by enhancing miR-223-3p to a certain extent. SIGNIFICANCE: This is novel research on the role of miR-223-3p in promoting radiotherapy resistance of PCa cells by activating glycolysis. This approach provides a new perspective and ideas for alleviating radiotherapy resistance of PCa cells.

Long non-coding RNA XIST promotes cell proliferation and migration through targeting miR-133a in bladder cancer.

The long non-coding RNA (lncRNA) X inactive specific transcript (XIST) has recently been reported to promote the malignant progression of bladder cancer through regulating several microRNAs (miRs), including miR-124, miR-139-5p and miR-200c. However, whether other miRs are also involved in this process has remained to be determined. The present study demonstrated that XIST was significantly upregulated in bladder cancer tissues compared with that in adjacent normal tissues. Furthermore, its expression was reduced in several common bladder cancer cell lines. High expression of XIST was significantly associated with tumour progression and poor prognosis of patients with bladder cancer. An in vitro experiment indicated that knockdown of XIST significantly reduced the proliferation and migration of bladder cancer cells. A luciferase assay suggested that XIST binds to its predicted binding site in miR-133a. In addition, it was identified that miR-133a was significantly downregulated in bladder cancer, and its expression levels were inversely correlated with those of XIST in bladder cancer tissues. Furthermore, loss- and gain-of-function experiments indicated that miR-133a acted as a downstream effector in XIST-mediated bladder cancer cell proliferation and migration. In conclusion, the present study demonstrates that XIST promotes bladder cancer cell proliferation and migration via targeting miR-133a and thus suggests that XIST may be used as a potential therapeutic target for bladder cancer.

miR-103a-2-5p/miR-30c-1-3p inhibits the progression of prostate cancer resistance to androgen ablation therapy via targeting androgen receptor variant 7.

Androgens and androgen receptors are vital factors involved in prostate cancer progression, and androgen ablation therapies are commonly used to treat advanced prostate cancer. However, the acquisition of androgen ablation therapy resistance remains a challenge. Recently, androgen receptor splicing variants lacking the ligand-binding domain have been reported to play a critical role in the acquisition of androgen ablation therapy resistance. In the present study, we revealed that the messenger RNA expression and the protein levels of an androgen receptor variant 7 (AR-V7) were higher in prostate cancer tissue samples and in the AR-positive prostate cancer cell line, VCaP. In contrast, microRNA (miR)-30c-1-3p/miR-103a-2-5p expression was significantly downregulated in tumor tissues and cells. miR-30c-1-3p/miR-103a-2-5p overexpression could inhibit AR-V7 expression, suppress VCaP cell growth, and inhibit AR-V7 downstream factor expression by directly targeting the 3'-untranslated region of AR-V7. Under enzalutamide (Enza) treatment, the effects of AR-V7 overexpression were the opposite of those of miR-103a-2-5p/miR-30c-1-3p overexpression; more importantly, the effects of miR-103a-2-5p/miR-30c-1-3p overexpression could be significantly reversed by AR-V7 overexpression under Enza. In summary, we demonstrated a novel mechanism of the miR-30c-1-3p/miR-103a-2-5p/AR-V7 axis modulating the cell proliferation of AR-positive prostate cancer cells via AR downstream targets. The clinical application of miR-30c-1-3p/miR-103a-2-5p needs further in vivo validation.

What Would a Suprapubic Catheter Indwelling for 4 Years Be Like? A Case Report.

A 35-year-old male of 165 cm height and weight of 65 kg, had a suprapubic catheter indwelling for 4 years without replacement for urethral stricture. The catheter became gradually obstructed, and urine leaked out around the suprapubic catheter. A lumbar abdominal distension, an inferior abdominal mass and renal failure prompted him to seek medical attention in our hospital in September 2018. This clinical case is hereby presented from 3 aspects of imaging, lab examination, and operation.

Metadherin regulates epithelial-mesenchymal transition in carcinoma.

Metadherin (MTDH) was first identified in primary human fetal astrocytes exposed to HIV-1 in 2002 and then recognized as an important oncogene mediating tumorigenesis, progression, invasiveness, and metastasis of carcinomas. Epithelial-mesenchymal transition (EMT) is a vital process in embryonic development, organ repair, and cancer progression. MTDH and EMT have also been proved to be related to the prognosis of patients with cancers. Recent studies reveal a relationship between MTDH overexpression and EMT in some malignancies. This review highlights the overexpression of MTDH and EMT in cancers and their correlations in clinical studies. Positive correlations have been established between MTDH and mesenchymal biomarkers, and negative correlations between MTDH and epithelial biomarkers have also been established. Furthermore, experiments reveal EMT regulated by MTDH, and some signal pathways have been established. Some anticancer drugs targeting MTDH and EMT are introduced in this review. Some perspectives concerning EMT regulation by MTDH are also presented in this review.

[Application of scrotoscope in the diagnosis and treatment of testicular and epididymal diseases].

OBJECTIVE: To evaluate the safety and efficacy of scrotoscope in diagnosis and treatment of testicular and epididymal diseases. METHODS: From September 2010 to March 2012, a total of 75 patients, aged 15-64 years (mean age is 42.4 years) were included in this study. Based on ultrasonagraphy before surgery, 12 cases were diagnosed as testicular torsion and 63 cases were diagnosed as epididymal mass. All the patients underwent scrotoscope examination or scrotoscope epididymectomy. A small scrotal incision of 1.0 cm was performed. Bluntly dissection was then performed through the scrotal layer until the tunica sac was disclosed. We used cystoscope or resectoscope as scrotoscope. Keeping the drip fusion of isotonic solution inflowing, the scrotum was maintained appropriate distended. The tunica sac wall including parietal and visceral tunica was checked. The testis, epididymis was then examined from the anterior, posterior and both lateral aspects to find out any potential pathology. The operation time of scrotoscope, postoperative complications, surgery record, ultrasound and pathology results were collected from medical record. Visual analog pain scale (range from 0 points to 10 points, 0 represent no pain, 10 represent the most severe pain) was used to assess scrotal pain. The postoperative complications, recurrence and pain relief were evaluated, the accuracy rates of the diagnosis was compared between scrotoscope and ultrasound based on pathology results. RESULTS: All the patients were successfully performed scrotoscope except one because of inflammatory adhesion. The average time of the operation was 34.3±5.8 minutes, and no serious complications, such as severe edema, hematoma, testicular hydrocele and wound infection occurred. The accuracy rate of scrotoscope and ultrasound for the diagnosis of testicular torsion was 100% vs. 66.7%, and the accuracy rate of scrotoscope and ultrasound for the diagnosis of epididymal mass was 76.2% vs. 58.7%. In the study, 63 patients received scrotoscope epididymectomy, the visual analogue pain score before surgery was 7.1±0.8, 6 months after operation, and the pain score was 2.4±0.6. CONCLUSION: Scrotoscope is safe. There are no serious complications such as severe edema, hematoma, testicular hydrocele and wound infection occurred. Scrotoscope is superior to ultrasound for diagnosis of testicular torsion and epididymal mass. Scrotoscope epididymectomy is effective for pain relief, especially for patients with epididymal cyst.

Comparison between Open Epididymal Cystectomy and Minimal Resection of Epididymal Cysts Using a Scrotoscope: A Clinical Trial for the Evaluation of a New Surgical Technique.

OBJECTIVE: To provide a new surgical technique for epididymal cyst (EC) treatment and to assess its safety and efficiency. METHODS: Forty-eight patients with symptomatic EC were randomized into 2 groups. One group (n = 23) received traditional open epididymal cystectomy (OEC) and the other group (n = 25) underwent minimal epididymal cystectomy with scrotoscope (MECS), which provided a clear vision of scrotal contents. Demographic information and perioperative and postoperative outcomes data were obtained and analyzed during a 2- to 6-month follow-up. RESULTS: No significant differences between the OEC and MECS groups were found in demographic information. Compared with OEC group, the MECS group had a shorter operating time (18.6 ± 2.9 vs 54.5 ± 7.0 minutes; P <.05), shorter incision length (1.1 ± 0.2 vs 4.8 ± 0.6 cm; P <.05), and less blood loss (4.6 ± 1.6 vs 17.0 ± 3.1 g; P <.05). Except for the 8.0% rate (2 of 25) of scrotal edema after MECS and 17.4% rate (4 of 23) of scrotal hematoma after OEC, both groups resulted in 0% incidence of testis or epididymis injury, wound infection, and cyst recurrence based on postoperative outcome data. Significant differences were observed after MECS compared with those after OEC based on the rates of symptom relief (95.2% vs 61.1%; P <.05) and days of wound pain (12.1 ± 2.6 vs 17.7 ± 4.1 days; P <.05). CONCLUSION: For the first time, our study applied scrotoscope as a new alternative technique for EC treatment. Scrotoscope provides a clear field of vision and makes tissues harvested available for pathologic examination when performing decortications of EC. The results suggest MECS may be a safe, effective, and encouraging new technique.

Micro-ribonucleic acid 29b inhibits cell proliferation and invasion and enhances cell apoptosis and chemotherapy effects of cisplatin via targeting of DNMT3b and AKT3 in prostate cancer.

BACKGROUND: Micro-ribonucleic acids (miRNAs) are crucial regulators in malignant tumors. miRNA-29b (miR-29b) has been identified as a tumor suppressor in prostate cancer (PCa). However, very few studies have investigated the effects of miR-29b in PCa, especially the mechanism and its association with chemotherapy. Our study aimed to explore the role and mechanism of miR-29b in PCa. MATERIALS AND METHODS: The expression levels of miR-29b were detected in ten clinical PCa specimens and four different PCa cell lines through quantitative real-time polymerase chain reaction. After miR-29b mimics and inhibitors were successfully transfected into LNCaP, the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was then used to investigate cell proliferation and cisplatin sensitivity of PCa cells. Cell cycle, cell apoptosis, and cell invasion were detected via flow cytometry, annexin V-fluorescein isothiocyanate labeling, and transwell assay, respectively. Based on bioinformatic methods, Western blot analysis, and dual-luciferase reporter assay, novel target genes of miR-29b were identified. RESULTS: miR-29b was downregulated in PCa tissues compared with matched adjacent nontumor tissues. In the androgen-independent PCa cell line (LNCaP-AI), the expression of miR-29b was much lower than the androgen-dependent PCa cell line (LNCaP). Subsequent studies showed that forced expression of miR-29b inhibited cell proliferation and cell invasion and induced cell apoptosis in PCa. Upregulation of miR-29b also enhanced the chemosensitivity of PCa cells to cisplatin. Moreover, we identified DNMT3b and AKT3 as novel target genes of miR-29b in PCa. CONCLUSION: Taken together, the results showed that miR-29b plays a tumor-suppressive role in PCa. It inhibits cell biological behavior and enhances the chemotherapy effects of cisplatin through its involvement in epigenetic regulation and PI3K/AKT pathway.

Association between benign prostatic hyperplasia, body mass index, and metabolic syndrome in Chinese men.

Previous studies have showed that men suffering from diabetes mellitus, metabolic syndrome (MetS) and obesity have a higher risk of benign prostatic hyperplasia (BPH). The present study aimed to examine the association between BPH, obesity, and features of MetS among men of the Hunan area of China. For this cross-sectional study, 904 males (aged 50-59 years) were included. MetS parameters, International Prostate Symptom Score (IPSS), prostate-specific antigen (PSA) levels, total prostate volume (TPV), postvoid residual volume (PVR) and maximum urine flow rate (Qmax) were measured. Results showed that MetS was associated with TPV (P = 0.048), PVR (P = 0.004) and IPSS (P = 0.011), but not with other indicators of BPH progression such as PSA levels or Qmax. MetS was associated with the voiding symptoms score (P < 0.05), but not with the storage symptom score. In addition, body mass index and fasting blood glucose positively correlated with TPV (r = 0.416, P< 0.001; and r = 0.310, P= 0.011, respectively). In conclusion, results suggest that MetS is associated with higher prostatic volume, prostate symptom score and voiding symptoms, but not with other features of prostatic hyperplasia such as PSA levels or Qmax. Changes in lifestyle factors, including physical activity and prevention of MetS, might be useful to prevent BPH and its progression, but further studies are needed.

Adult metastatic yolk sac tumor descending from an intra-abdominal testis: A case report and review of the literature.

Pure yolk sac tumors are extremely rare in adults; to the best of our knowledge, <20 cases have been reported. Multiple metastases originating from a pure yolk sac testicular tumor, descending from an intra-abdominal testis, are additionally extremely rare. In the present case, a man exhibiting a 30-year history of cryptorchidism and indirect inguinal hernia, was admitted to the Department of Urology (The Second Xiangya Hospital, Changsha, China) due to a mass that had descended from the abdominal cavity 7 months previously. Elevated levels of specific serum marker (α-fetoprotein, lactate dehydrogenase and human chorionic gonadotropin) did not indicate potential testicular germ cell types prior to surgery and pathological examination. Pathological results and immunohistochemistry revealed a testicular pure yolk sac tumor subsequent to surgery. The present case report and literature review describes the typical characteristics of an adult testicular yolk sac tumor, as well as the diagnosis and management of the disease.

MiR-223-3p targeting SEPT6 promotes the biological behavior of prostate cancer.

MicroRNAs (miRNAs) present frequently altered expression in urologic cancers including prostate, bladder, and kidney cancer. The altered expression of miR-223 has been reported in cancers and other diseases in recent researches. MiR-223 is up-regulated in systemic lupus erythematosus and rheumatoid arthritis. In neoplastic diseases, miR-223 is proved to be up-expressed in plasma or serum and cancer tissues compared with normal tissues in pancreatic cancer, gastric cancer, et al. However, whether altered expression of miR-223 is associated with prostate cancer (PCa) and what it is potential functions in PCa remained unveiled. In this study, we firstly found miR-223-3p were up-regulated in prostate cancer tissues and then we study functional role of miR-223-3p in PCa using DU145, PC3 and LNCaP cell lines. Our data suggested that miR-223-3p might target gene SEPT6 and promoted the biological behavior of prostate cancer. Notably, we found increasing SEPT6 expression might reverse the biological activity induced by miR-223-3p, which might be a potential therapeutic target for PCa.

Sugar signalling mediates cluster root formation and phosphorus starvation-induced gene expression in white lupin.

Cluster root (CR) formation contributes much to the adaptation to phosphorus (P) deficiency. CR formation by white lupin (Lupinus albus L.) is affected by the P-limiting level in shoots, but not in roots. Thus, shoot-derived signals have been expected to transmit the message of P-deficiency to stimulate CR formation. In this study, it is shown that sugars are required for a response to P starvation including CR formation and the expression of P starvation-induced genes. White lupin plants were grown in vitro on P-sufficient or P-deficient media supplemented with sucrose for 4 weeks. Sucrose supply stimulated CR formation in plants on both P-sufficient and P-deficient media, but no CR appeared on the P-sufficient medium without sucrose. Glucose and fructose also stimulated CR formation on the P-sufficient medium. On the medium with sucrose, a high concentration of inorganic phosphate in leaves did not suppress CR formation. Because sorbitol or organic acid in the media did not stimulate CR formation, the sucrose effect was not due to increased osmotic pressure or enriched energy source, that is, sucrose acted as a signal. Gene transcription induced by P starvation, LaPT1 and LaPEPC3, was magnified by the combination of P limitation and sucrose feeding, and that of LaSAP was stimulated by sucrose supply independently of P supply. These results suggest that at least two sugar-signalling mediating systems control P starvation responses in white lupin roots. One system regulates CR formation and LaSAP expression, which acts even when P is sufficient if roots receive sugar as a signal. The other system controls LaPT1 and LaPEPC3 expression, which acts when P is insufficient.