Synthesis of Chiral Sulfoxides by A Cyclic Oxidation-Reduction Multi-Enzymatic Cascade Biocatalysis.

Optically pure sulfoxides are valuable organosulfur compounds extensively employed in medicinal and organic synthesis. In this study, we present a biocatalytic oxidation-reduction cascade system designed for the preparation of enantiopure sulfoxides. The system involves the cooperation of a low-enantioselective chimeric oxidase SMO (styrene monooxygenase) with a high-enantioselective reductase MsrA (methionine sulfoxide reductase A), facilitating "non-selective oxidation and selective reduction" cycles for prochiral sulfide oxidation. The regeneration of requisite cofactors for MsrA and SMO was achieved via a cascade catalysis process involving three auxiliary enzymes, sustained by cost-effective D-glucose. Under the optimal reaction conditions, a series of heteroaryl alkyl, aryl alkyl and dialkyl sulfoxides in R configuration were synthesized through this "one-pot, one step" cascade reaction. The obtained compounds exhibited high yields of >90 % and demonstrated enantiomeric excess (ee) values exceeding 90 %. This study represents an unconventional and efficient biocatalytic way in utilizing the low-enantioselective oxidase for the synthesis of enantiopure sulfoxides.

Kinetic resolution of sulfoxides with high enantioselectivity using a new homologue of methionine sulfoxide reductase B.

Optically pure sulfoxides are noteworthy compounds that find wide applications in various industrial fields. Here, we report a methionine sulfoxide reductase B (MsrB) homologue that exhibits high enantioselectivity and broad substrate scope for the kinetic resolution of racemic (rac) sulfoxides. This MsrB homologue, named liMsrB, was identified from Limnohabitans sp. 103DPR2 and showed good activity together with enantioselectivity towards a series of aromatic, heteroaromatic, alkyl and thioalkyl sulfoxides. Chiral sulfoxides in the S configuration were prepared in approximately 50% yield and 92-99% enantiomeric excess through kinetic resolution at an initial substrate concentration of up to 90 mM (11.2 g L-1). This study presents an efficient route for the enzymatic preparation of (S)-sulfoxides through kinetic resolution.

Risk factors for kidney stone disease recurrence: a comprehensive meta-analysis.

BACKGROUND: Kidney stone disease (KSD) is a common illness that causes an economic burden globally. It is easy for patients to relapse once they have suffered from this disease. The reported recurrence rate of KSD ranged from 6.1% to 66.9%. We performed this meta-analysis to identify various potential risk factors for the recurrence of KSD. METHODS: The PubMed, Embase and Web of Science databases were searched using suitable keywords from inception to Mar 2022. A total of 2,663 records were collected initially. After screening the literature according to the inclusion and exclusion criteria, 53 articles (40 retrospective studies; 13 prospective studies) including 488,130 patients were enrolled. The study protocol was registered with PROSPERO (No. CRD42020171771). RESULTS: The pooled results indicated that 12 risk factors including younger age (n = 18), higher BMI (n = 16), family history of kidney stones (n = 12), personal history of kidney stones (n = 11), hypertension (n = 5), uric acid stone (n = 4), race of Caucasian (n = 3), suspected kidney stone episode before the first confirmed stone episode (n = 3), surgery (n = 3), any concurrent asymptomatic (nonobstructing) stone (n = 2), pelvic or lower pole kidney stone (n = 2), and 24 h urine test completion (n = 2) were identified to be associated with KSD recurrence. In the subgroup analysis, patients with higher BMI (OR = 1.062), personal history of nephrolithiasis (OR = 1.402), or surgery (OR = 3.178) had a higher risk of radiographic KSD recurrence. CONCLUSIONS: We identified 12 risk factors related to the recurrence of KSD. The results of this analysis could serve to construct recurrence prediction models. It could also supply a basis for preventing the recurrence of KSD.

A new approach for reducing pollutants level: a longitudinal cohort study of physical exercises in young people.

BACKGROUND: The present study aimed to evaluate the elimination of three common pollutants (dimethoate, benzo(a)pyrene (BaP) and bisphenol A (BPA) by different physical exercises and to assess the possible factors which could affect the pollutants elimination. METHODS: A total of 200 individuals who chose different kinds of exercises in accordance to their own wish were recruited. The levels of urinary pollutants were measured using ß-glucuronidase hydrolysis followed by a high-performance liquid chromatography tandem mass spectrometry-based method. RESULTS: Totally, the levels of dimethoate, BaP and BPA were reduced after physical exercises. However, the elimination of BaP in male was higher than that in female but the elimination of BPA in female was higher than that in male. Multivariate logistic regression showed that the degree of heart rate (HR) change was a protective factor affecting the improvement effect of dimethoate, BaP and BPA while BMI (body mass index) was a risk factor. Nevertheless, sex was a risk factor affecting the improvement of dimethoate and BaP but had a lower efficacy on BPA improvement. CONCLUSION: The present findings indicate that physical exercises can be considered as a novel approach to eliminate pollutants level in human body and can also give suggestions for choosing specific physical exercises to male and female individuals. Moreover, those who are with higher BMI need to lose weight before eliminating pollutant level through physical exercises.

Urinary levels of dimethoate, bisphenol A and benzo[a]pyrene in first-year students of Hohai University from different geographical regions.

BACKGROUND: The objective of this study was to detect the urinary levels of dimethoate, benzo(a) pyrene (BaP), and bisphenol A (BPA) in first-year Hohai University students with different geographic origins. METHODS: First-morning urine samples were collected from 540 healthy freshmen aged 17 to 19 years. Chemical levels were measured using ß-glucuronidase hydrolysis followed by a high-performance liquid chromatography-tandem mass spectrometry-based method. Geometric means (GMs) of these three chemicals are presented by body mass index (BMI) and location in a volume-based and creatinine-standardized way. RESULTS: GM concentrations of omethoate, BPA and 3-OHBaP were 9.47 µg/L (10.80 µg/g creatinine), 3.54 µg/L (4.04 µg/g creatinine) and 0.34 ng/L (0.39 ng/g creatinine), respectively. The GM concentration of omethoate in males was significantly higher than that in females. The individuals with a BMI higher than 23.9 had higher GM concentrations of omethoate, BPA, and 3-OHBaP. The inhabitants of Southwest China had significantly lower GM concentrations of omethoate, BPA, and 3-OHBaP than those who lived in other locations in China. CONCLUSION: The average level of environmental chemical accumulation in freshmen is lower in Southwest China and differs in youth who live in different regions. In addition, obesity is correlated with higher toxin levels in youth.

Resveratrol inhibits the tumor migration and invasion by upregulating TET1 and reducing TIMP2/3 methylation in prostate carcinoma cells.

BACKGROUND: Recently, resveratrol (Res) has been suggested to suppress the migration and invasion of prostate cancer (PCa). In the present study, we aimed to investigate the effects of Res on genomic DNA methylation, as well as the migration and invasion of PCa cells. METHODS: The suppression by Res of the growth of PCa cells was verified through a cytotoxicity assay. In addition, the effects of Res on 5-methylcytosine (5mC), 5-hydroxymethylcytosine (5hmC), and ten-eleven translocation 1 (TET1) levels were assessed, and the cell migration and invasion were also determined. The expressions of TET1, tissue inhibitor of metalloproteinases (TIMP) 2, TIMP3, MMP2, and MMP9 were detected through Western blot analysis. Afterward, TET1 was silenced using lentiviral short hairpin RNA to examine the effect of TET1 on the Res-triggered inhibition of migration and invasion of PCa cells. RESULTS: Our results showed that Res upregulated the 5hmC and TET1 levels and downregulated the 5mC level. Moreover, Res also inhibited the migration and invasion of PCa cells, promoted the demethylation of TIMP2 and TIMP3 to upregulate their expressions, and suppressed the expressions of MMP2 and MMP9. The silencing of TET1 in the presence of Res showed that Res could exert its effect through TET1. CONCLUSIONS: Our findings indicated that Res inhibited the migration and invasion of PCa cells via the TET1/TIMP2/TIMP3 pathway, which might potentially serve as a target for the treatment of PCa.

Upregulated immune checkpoint HHLA2 in clear cell renal cell carcinoma: a novel prognostic biomarker and potential therapeutic target.

BACKGROUND: Clear cell renal cell carcinoma (ccRCC) is a malignant urogenital cancer with high mortality; however, current progress in understanding its molecular mechanism and predicting clinical treatment outcome is limited. Therefore, this study is to evaluate the clinical significance of immune inhibitory molecular human endogenous retrovirus-H long terminal repeat-associating protein 2 (HHLA2) in ccRCC prognosis and transcriptional regulatory network. METHODS: Expression of HHLA2 in ccRCC was examined by an online database platform ONCOMINE. The ONCOMINE result was independently validated by qRT-PCR and immunohistochemistry. Kaplan-Meier survival was generated using IBM SPSS Statistics V.22. ccRCC tissues cells with high HHLA2 were sorted and subjected to microarray transcriptional profiling and analysis. RESULTS: It was shown that expression of HHLA2 was statistically significantly increased in ccRCC tissues compared with normal renal tissues at both transcriptional and protein level. Moreover, the expression of HHLA2 was closely correlated with multiple clinicopathological features including tumour size, clinical stage and histological grade. High HHLA2 expression was associated with poor overall survival and clinical outcome. Comprehensive microarray analysis further identified thousands of HHLA2 targets including mRNA, long non-coding RNA and circular RNA that might function in various biological processes, especially, immune response. CONCLUSION: Increased HHLA2 expression was observed in ccRCC tumour tissue, which leads to a remarkable shorter overall survival and poorer prognosis. Together with other molecular evidence, we have demonstrated that HHLA2 could be a potential prognostic biomarker for ccRCC.

LINC00961 restrains cancer progression via modulating epithelial-mesenchymal transition in renal cell carcinoma.

Recently, long noncoding RNA have been identified as new gene regulators and prognostic biomarkers in various cancers, including renal cell carcinoma (RCC). The expression and biological roles of LINC00961 have been reported in many human cancers. However, up to date, no study of LINC00961 has been shown in RCC. Currently, we aimed to investigate the function of LINC00961 in RCC progression. Interestingly, we observed that LINC00961 could act as a novel biomarker in predicting the diagnosis of RCC. Then, we found that LINC00961 was greatly downregulated in RCC cell lines (Caki-1, Caki-2, 786-O, A498, and ACHN cells) compared with normal renal cell lines (HK-2 cells). Then, 786-O cells and ACHN cells were infected with LV-LINC00961. As displayed in our current study, LINC00961 overexpression could obviously suppress the proliferation and survival of RCC cells in vitro. In addition, RCC cell apoptosis was greatly induced and cell cycle progression was blocked in G1 phase by upregulation of LINC00961 in 786-O cells and ACHN cells. Subsequently, we found that LV-LINC00961 was able to restrain RCC cell migration and cell invasion capacity. Meanwhile, the messenger RNA and protein expression levels of epithelial-mesenchymal transition (EMT)-associated markers Slug and N-cadherin in RCC cell lines were dramatically inhibited by overexpressing LINC00961. Finally, the in vivo experiment was carried out and we observed that LINC00961 could inhibit RCC development through modulating EMT process. Taken these together, it was indicated in our study that LINC00961 was involved in RCC progression through targeting EMT pathway.

Mechanisms of Paeonia lactiflora in Treatment of Ulcerative Colitis: A Network Pharmacological Study.

BACKGROUND Paeonia lactiflora is the main active ingredient of peony decoction, which is used to treat ulcerative colitis (UC) in traditional Chinese medicine (TCM). Network pharmacology indicates the multiple interactions among genes, proteins, and metabolites associated with diseases and drugs from the network perspective, which shows the multi-component and multi-target attributes of TCM. This study predicted the pharmacological mechanism of Paeonia lactiflora in the treatment of UC by network pharmacological method. MATERIAL AND METHODS Chemical constituents of Paeonia lactiflora were searched from TCMSP data, gene names of target sites were extracted from UniProt database, and disease targets of ulcerative colitis were obtained from the CTD disease database. Use Venny online tools to obtain common targets for drugs and diseases. The DAVID database was used to enrich GO and KEGG for the common target, and the related functions and pathways were obtained. Cytoscape 3.7.1 was used to construct the 'drug-compound-target-disease' network. RESULTS There are 70 common target genes between Paeonia lactiflora and UC. GO analysis showed that the biological functions of the common target genes of Paeonia lactiflora and UC include response to lipopolysaccharide, response to estradiol, response to drug, positive regulation of nitric oxide biosynthetic process, and steroid hormone-mediated signaling pathway. Enrichment of the KEGG signaling pathway mainly involves signaling pathways, including Pathways in cancer, TNF signaling pathway, Tuberculosis, Hepatitis B, and Toxoplasmosis. CONCLUSIONS The network pharmacology intuitively shows the multi-component, multi-target, and multi-channel pharmacological effects of Paeonia lactiflora on UC, and provides a scientific basis for studying the mechanism of the effect of Paeonia lactiflora on UC.

Mediating Roles of Anxiety, Self-Efficacy, and Sleep Quality on the Relationship Between Patient-Reported Physician Empathy and Inflammatory Markers in Ulcerative Colitis Patients.

BACKGROUND Empathy between doctor and patient has an important bearing on patient health. The purpose of this study was to assess whether anxiety, sleep quality, and self-efficacy of patients have mediating effects in the relationship of patient-reported physician empathy and inflammatory factor in ulcerative colitis (UC) patients. MATERIAL AND METHODS This study included 242 patients attended by 45 doctors. Self-reported doctors' empathy ability was measured at patient admission (T1), and patient-reported physician empathy was measured 3 months later (T2). Patient anxiety, general self-efficacy, sleep, and inflammatory factor (IL-6) were measured on T1 and T2. Pearson correlation analysis was used to assess the relationships between self-reported doctor empathy ability and patient indices on T1 and T2. The relationships between anxiety, sleep quality, self-efficacy, IL-6, and patient-reported physician empathy were measured by Pearson correlation analysis and structural equation modeling. RESULTS On T1, no significant correlation was reported between self-reported doctors' empathy ability and indices of the patients (P>0.05). On T2, self-reported doctors' empathy ability was significantly positively correlated with patient sleep and self-efficacy (P<0.01), and significantly negatively correlated with patient anxiety and IL-6 (P<0.01). Moreover, on T2, patient-reported physician empathy was negatively correlated with anxiety and IL-6 and was positively correlated with self-efficacy and sleep quality. The effect of patient-reported physician empathy on IL-6 was mediated by anxiety, sleep quality, and self-efficacy. CONCLUSIONS The anxiety, self-efficacy, and sleep quality of UC patients had mediating effects in the relationship between patient-reported physician empathy and IL-6.

Prognostic Role of High Gal-9 Expression in Solid Tumours: a Meta-Analysis.

BACKGROUND/AIMS: Recently, many studies have demonstrated that galectin-9 (Gal-9) exhibits altered expression and has a close association with metastasis and recurrence in various cancers. Therefore, we conducted a meta-analysis to assess the prognostic role of Gal-9 expression in solid tumours. METHODS: We searched PubMed, Embase, and Web of Science until June 2017 and identified fourteen eligible studies containing 2,408 patients to include in the meta-analysis. RESULTS: The pooled results indicated that higher Gal-9 expression in cancer tissue associated with an improved CSS (HR=0.48, 95% CI 0.39-0.58). In the subgroup analysis, a significant relationship was observed between higher Gal-9 expression and both CSS (HR=0.48, 95% CI 0.39-0.59) and OS (HR=0.62, 95% CI 0.49-0.78) in digestive cancers. CONCLUSIONS: The findings of this meta-analysis highlight the role of Gal-9 as a useful clinical prognostic biomarker, which may facilitate the treatment of patients with solid tumours.

Prognostic significance of galectin-1 expression in patients with cancer: a meta-analysis.

BACKGROUND: The prognostic significance of galectin-1 (Gal-1) expression in cancerous patients has been assessed for several years while the results remain controversial. Thus, we performed the first comprehensive meta-analysis to evaluate the prognostic value of Gal-1 expression in cancerous patients. METHODS: We searched Pubmed, Embase and Web of Science to recruit studies on the prognostic impact of Gal-1 expression in cancerous patients. Eighteen studies containing 2674 patients were involved in this meta-analysis until March 30, 2018. Pooled hazard ratios (HRs) with 95% confidence interval (95% CI) were calculated to estimate the effect using random-effects model. RESULTS: The pooled results revealed that high Gal-1 expression in cancer tissue associated with a poor OS (HR = 1.79, 95% CI 1.54-2.08, P < 0.001). In the subgroup of tumor type, it's observed that high Gal-1 expression was significant correlated with poor OS in digestive cancers without heterogeneity (HR = 1.94, 95% CI 1.64-2.30, P < 0.001; fixed-effects model; I2 = 20.1%, P = 0.276). CONCLUSIONS: Our present meta-analysis indicates that high Gal-1 expression might be a predictive factor of poor prognosis in cancers, particularly in digestive cancers.

Hierarchical fibrous microfiltration membranes by self-assembling DBS nanofibrils in solution-blown nanofibers.

A novel hierarchical nanofibrous membrane was demonstrated via in situ self-assembly of 1,3:2,4-dibenzylidene-d-sorbitol (DBS) supramolecular fibrils in solution-blown polyacrylonitrile (PAN) nanofibers. The formed DBS fibrils were interconnected into networks and anchored onto the PAN nanofibers, which decreased the pore sizes and enhanced the mechanical properties, the filtration efficiency, and particularly the flux.

Induction therapy of basiliximab versus antithymocyte globulin in renal allograft: a systematic review and meta-analysis.

OBJECTIVE: The aim of this meta-analysis was to evaluate the efficacy of basiliximab versus antithymocyte globulin for induction therapy in renal allograft. METHODS: Medline (PubMed), Embase, Ovid, Cochrane, and the Chinese Biomedical Literature databases were searched to identify prospective randomized controlled trials that compared basiliximab with antithymocyte globulin (ATG) for induction therapy in renal transplantation. RevMan 5.1 software and Stat Manager V4.1 software were used for the meta-analysis. RESULTS: Eight RCTs were included, including a total of 1153 patients. Of these, 547 (47%) had received basiliximab, and 606 (53%) had received ATG. The pooled results revealed that the basiliximab had a lower rate of neoplasm compared with ATG [odds ratio (OR) 0.26; 95% confidence interval (CI) 0.08-0.78; P = 0.02]. There were no significant differences between the two drugs regarding 1-year acute rejection rate (OR 1.32; 95% CI 0.93-1.87; P = 0.13), 1-year graft survival rate (OR 0.73; 95% CI 0.45-1.18; P = 0.20), 1-year patient survival rate (OR 0.52; 95% CI 0.27-1.02; P = 0.06), 1-year infection rate (OR 0.90; 95% CI 0.48-1.68; P = 0.73). CONCLUSION: Induction therapy of basiliximab has similar short-time effects on the recipients in renal transplantation compared with that of ATG. However, regarding the long-term effect, as represented by the rate of neoplasm, basiliximab has a significant advantage.

Night-time blood pressure and pulse wave velocity in dialysis patients.

BACKGROUND: Ambulatory blood pressure (ABP) monitoring and carotid-femoral pulse wave velocity (cfPWV) provide important cardiovascular risk information for dialysis patients. This study aims to evaluate the risk factors of cfPWV and the associations between ambulatory blood pressure, especially night-time blood pressure and cfPWV. METHODS: We conducted a cross-sectional study in patients on maintenance hemodialysis. ABP and cfPWV were measured on a midweek interdialytic day. Associations were determined using Pearson's correlation analysis and multiple stepwise regression model. RESULTS: Systolic BPs and pulse pressures, but not diastolic BPs, were significantly and positively associated with cfPWV. In a stepwise regression model, age, diabetes mellitus and all-period systolic BP were independently associated with cfPWV. When day-time and night-time BPs were included in the analysis, respectively, only night-time systolic BP and age remained as independently associated with cfPWV. CONCLUSION: Ambulatory BPs are potent associates of cfPWV and night-time systolic BP, rather than day-time BPs, is an independently predictor of cfPWV. Our results support the view that controlling of nocturnal hypertension provides a unique cardiovascular protection effect.

Hydrogen Rich Water Attenuates Renal Injury and Fibrosis by Regulation Transforming Growth Factor-ß Induced Sirt1.

The current research was designed to study the role of hydrogen in renal fibrosis and the renal epithelial to mesenchymal transition (EMT) induced by transforming growth factor-ß1 (TGF-ß1). Hydrogen rich water (HW) was used to treat animal and cell models. Unilateral ureteral obstruction (UUO) was performed on Balb/c mice to create a model of renal fibrosis. Human kidney proximal tubular epithelial cells (HK-2 cells) were treated with TGF-ß1 for 36 h to induce EMT. Serum creatinine (Scr) and blood urea nitrogen (BUN) were measured to test renal function, in addition, kidney histology and immunohistochemical staining of alpha-smooth muscle actin (α-SMA) positive cells was performed to examine the morphological changes. The treatment with UUO induced a robust fibrosis of renal interstitium, shrink of glomerulus and partial fracture of basement membrane. Renal function was also impaired in the experimental group with UUO, with an increase of Scr and BUN in serum. After that, Western-blot was performed to examine the expression of α-SMA, fibronectin, E-cadherin, Smad2 and Sirtuin-1 (Sirt1). The treatment with HW attenuated the development of fibrosis and deterioration of renal function in UUO model. In HK-2 cells, the pretreatment of HW abolished EMT induced by TGF-ß1. The down-regulation the expression of Sirt1 induced by TGF-ß1 which was dampened by the treatment with HW. Sirtinol, a Sirt1 inhibitor, reversed the effect of HW on EMT induced by TGF-ß1. HW can inhibit the development of fibrosis in kidney and prevents HK-2 cells from undergoing EMT which is mediated through Sirt1, a downstream molecule of TGF-ß1.

Berberine Improved Aldo-Induced Podocyte Injury via Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress Pathways both In Vivo and In Vitro.

BACKGROUND/AIMS: Berberine, a naturally occurring isoquinoline alkaloid, acts against oxidative stress (OS) and endoplasmic reticulum stress (ERS), both of which are responsible for Aldosterone (Aldo) -induced podocyte injury. However, the direct effects of berberine on Aldo-induced OS, ERS, and podocyte injury are not well defined. METHODS: Uninephrectomized Sprague-Dawley rats were given 1% NaCl (salt) in their water and an Aldo infusion (0.75 µg/h) for 28 days to induce podocyte injury in the Aldo group. In the Aldo/berberine group, in addition to Aldo infusion, rats were administered 150 mg/kg berberine per day by gastric gavage for 4 weeks. Podocytes were incubated in media containing either buffer or Aldo in the presence or absence of berberine for variable time periods. The kidney tissues and podocytes were then investigated using morphological analysis, immunohistochemistry, transmission electron microscopy, western blot, DHE staining, DCFDA fluorescence, and Annexin V staining. RESULTS: Here, we have reported that berberine attenuated Aldo-induced OS, ERS, and podocyte injury both in vivo and in vitro. Additionally, berberine treatment improved the extensive fusion of foot processes in electron micrographs resulting from Aldo/salt infusion in rats. CONCLUSION: Berberine may be examined as an effective agent against Aldo-induced podocyte injury.

Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy.

Tissue hypoxia/ischemia is a pathological feature of many human disorders including stroke, myocardial infarction, hypoxic/ischemic nephropathy, as well as cancer. In the kidney, the combination of limited oxygen supply to the tissues and high oxygen demand is considered the main reason for the susceptibility of the kidney to hypoxic/ischemic injury. In recent years, increasing evidence has indicated that a reduction in renal oxygen tension/blood supply plays an important role in acute kidney injury, chronic kidney disease, and renal tumorigenesis. However, the underlying signaling mechanisms, whereby hypoxia alters cellular behaviors, remain poorly understood. Mitogen-activated protein kinases (MAPKs) are key signal-transducing enzymes activated by a wide range of extracellular stimuli, including hypoxia/ischemia. There are four major family members of MAPKs: the extracellular signal-regulated kinases-1 and -2 (ERK1/2), the c-Jun N-terminal kinases (JNK), p38 MAPKs, and extracellular signal-regulated kinase-5 (ERK5/BMK1). Recent studies, including ours, suggest that these MAPKs are differentially involved in renal responses to hypoxic/ischemic stress. This review will discuss their changes in hypoxic/ischemic pathophysiology with acute kidney injury, chronic kidney diseases and renal carcinoma.

LncRNA GAS5 inhibits proliferation and progression of prostate cancer by targeting miR-103 through AKT/mTOR signaling pathway.

In prior research, evidence has been found for a relation between low exposure of long non-coding RNAs (lncRNAs) and prostate tumor genesis. This study aims to clarify the underlying mechanisms of lncRNA GAS5 in prostate cancer (PCa). In total, 118 pairs of PCa tissues and matched adjacent non-tumor tissues were collected. Additionally, lncRNA GAS5 exposure levels were determined using RT-PCR and in situ hybridization. In addition, dual-luciferase report assay was performed to verify the target effect of lncRNA GAS5 on miR-103. The exposure levels of the proteins related to the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) axis, including AKT, mTOR, and S6K1, were measured by western blot PC3 cells infected with lncRNA GAS5 mimic; lncRNA GAS5 siRNA; or a combination of lncRNA and miR-103. The proliferation, invasion, and migration ability of PC3 cells after being infected were tested by MTT assay, wound healing assay, and transwell assays. Finally, nude mouse xenograft models were used to measure lncRNA GAS5 effects on prostate tumor growth in vivo. The lncRNA GAS5 levels were reduced significantly in the PCa tissues and cell lines (P < 0.05). A low exposure of lncRNA GAS5 caused AKT/mTOR signaling pathway activation in PC3 cells (P < 0.05). In addition, over-exposure of lncRNA GAS5 was proven to significantly decelerate PCa cell progression in vitro and tumor growth in vivo through inactivating the AKT/mTOR signaling pathway (P < 0.05). This study proves that lncRNA GAS5 plays a significant role in the decelerating PCa development via mediating the AKT/mTOR signaling pathway through targeting miR-103.