LncRNA-MALAT1 Regulates Cancer Glucose Metabolism in Prostate Cancer via MYBL2/mTOR Axis.

It is known that the long noncoding RNAs (lncRNA) MALAT1 is associated with tumorigenesis and progression in various cancers; however, its functions and mechanisms in prostate cancer (PCa) initiation and progression are still unknown. In the present study, our findings revealed that MALAT1 plays a critical part in regulating PCa proliferation and glucose metabolism. Knockdown of MALAT1 affects the protein and mRNA levels of MYBL2. In addition, MALAT1 enhances the phosphorylation level of mTOR pathway by upregulating MYBL2. Knockdown of MALAT1 or MYBL2 in PCa cell lines significantly inhibits their proliferation capacity. Silencing MALAT1/MYBL2/mTOR axis in PCa cell lines affects their glycolysis and lactate levels, and we verified these findings in mice. Furthermore, we explored the underlying tumorigenesis functions of MYBL2 in PCa and found that high expression of MYBL2 was positively associated with TNM stage, Gleason score, PSA level, and poor survival rate in PCa patients. Taken together, our research suggests that MALAT1 controls cancer glucose metabolism and progression by upregulating MYBL2-mTOR axis.

[Correlation of the platelet count in the peripheral blood with the prostate volume].

OBJECTIVE: To investigate the relationship of the prostate volume with the count of inflammatory cells in the peripheral blood and clarify the pathogenesis of BPH. METHODS: From 2015 to 2019, we enrolled 104 men pathologically diagnosed with BPH. Using univariate and multivariate linear regression analysis models, we analyzed the correlation of the prostate volume with the neutrophil count, platelet count, neutrophil-lymphocyte ratio (NLR), platelet-WBC ratio (PWR), and lymphocyte-monocyte ratio (LMR) in the peripheral blood of the patients. RESULTS: Both the platelet count (r = 0.401, P < 0.001) and PWR (r = 0.343, P < 0.001) in the peripheral blood were positively correlated with the prostate volume and serum PSA level, but not with IPSS. No evident relationship was found between the prostate volume and the systemic inflammatory markers NLR and LMR. CONCLUSIONS: The platelet count in the peripheral blood is an important predictor of BPH and may play an important role in the development and progression of BPH.

5-aminolevulinic acid photodynamic therapy and holmium laser treatment for intraurethral condylomata acuminata in a renal transplant patient.

Condylomata acuminata (CA) caused by human papillomavirus, often involves the external genitalia, perianal skin, and other moist mucous membranes. Urethral involvement is uncommon and little recognized, and usually limited to the distal 3 cm of the meatus. It is difficult to treat CA involving the urethra because of the anatomical location, risk of complications and recurrence. One effective method for the treatment of CA located at the urinary meatus is 5-aminolevulinic acid photodynamic therapy (ALA-PDT). However, experience of using this method for the treatment of whole urethral CA is still very limited. Herein, we treated a whole urethral CA successfully with photodynamic and holmium laser therapies. The case of a 25-year-old patient who underwent kidney transplant effected by intraurethral CA is presented and discussed. Catheter implantation and (or) immunosuppression treatment increases the risk of urethral condyloma acuminatum. The ALA-PDT is a safe, straightforward, effective, and well-tolerated treatment procedure for intraurethral CA. ALA-PDT combined with holmium laser treatment can successfully treat kidney transplant patients with intraurethral CA.

Establishment of animal model manifested as bladder neurogenic changes generated by bilateral pelvic nerve injury in male rats.

PURPOSE: To establish a male rat model of neurogenic bladder after bilateral pelvic nerve injury (BPNI) and investigate the factors associated with onset of neurogenic bladder. METHODS: Twenty-four 8-week-old male Sprague-Dawley rats were randomly divided into three groups (n = 8 rats per group). Rats in 4-week and 8-week nerve injury group underwent BPNI, while rats in the sham group underwent a sham operation. Bladder functional analysis were performed and then bladders tissues were harvested for morphological examination and investigating the mRNA expression levels of target genes in all rats. RESULTS: The bladder weight significantly increased in rats following BPNI. Functional analysis revealed non-voiding contractions and decreased detrusor contractility following BPNI, manifested as elevated post-void residual and bladder capacity while reduced maximum voiding pressure and voiding efficiency. The collagen area in bladder tissue and mRNA expression levels of target genes significantly increased at 4 or 8 weeks post-BPNI except Smad3. At 4 weeks post-BPNI, expression levels of vesicular acetylcholine transporter were reduced, then returned to baseline at 8 weeks. Expression levels of tyrosine hydroxylase were reduced at both 4 and 8 weeks post-BPNI. CONCLUSIONS: A neurogenic bladder animal model was successfully established by performing BPNI in male rats, characterized by impaired voiding function, bladder detrusor fibrosis, and reduced neurotransmitter release.

Study on the Effect of Polymer Nano-Loaded Drug System on Bladder Cancer Perfusion.

Bladder tumor is a malignant tumor on bladder mucosa and the most common malignant tumor of urinary system. At present, bladder cancer is mainly treated by surgical resection and intravesical infusion of anticancer drugs. The high-molecular nano-drug-loading system has the advantages of direct focus of the drug in the treatment of cancer, reduced systemic toxicity and high local concentration. The purpose of this paper was to study the effect of polymer nano-drug loading system on bladder cancer perfusion. The synthesized polymer was applied to the establishedmouse bladder cancer model, the anticancer effect of polymer nano-drug loading system on mice in vivo was observed, and the health status of mice during administration was determined. It was found that a large number of drugs could adhere to the tumor tissue after perfusion of bladder cancer with polymer nano-drug loading system, and the effect of killing bladder cancer cells was better.

miR­22­3p enhances multi­chemoresistance by targeting NET1 in bladder cancer cells.

With the discovery of new chemotherapeutic drugs, chemotherapy becomes increasingly valuable. However, the resistance of tumor cells to chemotherapeutic agents significantly limits the effectiveness and causes chemotherapy failure. MicroRNAs have been shown to regulate drug resistance in many types of cancer. In the present study, we measured the chemosensitivity of five bladder cancer (BCa) cell lines to seven commonly used chemotherapeutic drugs by Vita­Blue assay. We then identified the most sensitive (5637) and most tolerant cell lines (H­bc) and conducted a multi­group test. This test included expression group analyses of coding and non­coding genes (miR­omic and RNA­seq). Based on our analyses, we selected miR­22­3p as a target. We then determined its own target gene [neuroepithelial cell transforming 1 (NET1)] by bioinformatic analysis and confirmed this finding by TaqMan­quantitative reverse transcription polymerase chain reaction (qRT­PCR), western blot analysis and luciferase reporter assay. The effect of miR­22­3p on BCa multi­chemoresistance was also determined by transfecting cells with the miR­22­3p­mimic or miR­22­3p­antagomiR. We assessed the involvement of NET1 in BCa chemoresistance by siRNA­mediated NET1 inhibition or pINDUCER21­enhanced green fluorescent protein­NET1­mediated overexpression. Plate colony formation and apoptosis assays were conducted to observe the effects of miR­22­3p and NET1 on BCa chemoresistance. In conclusion, our results suggest that miR­22­3p promotes BCa chemoresistance by targeting NET1 and may serve as a new prognostic biomarker for BCa patients.

Effects of metformin on prostatic tissue of rats with metabolic syndrome and benign prostatic hyperplasia.

OBJECTIVES: To investigate the efficacy of insulin sensitizer on prostatic tissue in animal model with benign prostatic hyperplasia (BPH) secondary to metabolic syndrome (MetS). METHODS: Models were established by providing Sprague-Dawley rats with high fat diet (HFD) combined with metformin or not. All objects were killed 40 days later with prostatic tissue being removed, weighed before stained, as well as the expression level of insulin-like growth factor I (IGF-1) and receptor (IGF-1R) being measured, and the level of insulin resistance (IR) has also been evaluated. RESULTS: Model has been successfully established. Level of prostatic hyperplasia and IR as well as IGF-1 and IGF-1R expressions in the blank and saline control subunits of HFD group was higher than that of normal diet group (P < 0.05). In the subunit of metformin, along with the suppression of IR, the level of prostatic hyperplasia and the expression of IGF-1 pathway have both decreased (P < 0.05). CONCLUSION: MetS can promote the growth of prostate during the formation of central obesity and IR. IGF-1 pathway may have an important role in the induction of BPH following IR. The application of metformin can suppress the expression of IGF-1 and IGF-1R, thus preventing the promotive effect of IR on prostate tissue in animal model of MetS.