Shen Yuan extract exerts a hypnotic effect via the tryptophan/5-hydroxytryptamine/melatonin pathway in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Sleep plays a critical role in several physiologic processes, and sleep disorders increase the risk of depression, dementia, stroke, cancer, and other diseases. Stress is one of the main causes of sleep disorders. Ginseng Radix et Rhizoma and Polygalae Radix have been reported to have effects of calming the mind and intensifying intelligence in Chinese Pharmacopoeia. Traditional Chinese medicine prescriptions composed of Ginseng Radix et Rhizoma and Polygalae Radix (Shen Yuan, SY) are commonly used to treat insomnia, depression, and other psychiatric disorders in clinical practice. Unfortunately, the underlying mechanisms of the SY extract's effect on sleep are still unknown. AIM OF THE STUDY: This study aimed to investigate the hypnotic effect of the SY extract in normal mice and mice with chronic restraint stress (CRS)-induced sleep disorders and elucidate the underlying mechanisms. MATERIALS AND METHODS: The SY extract (0.5 and 1.0 g/kg) was intragastrically administered to normal mice for 1, 14, and 28 days and to CRS-treated mice for 28 days. The open field test (OFT) and pentobarbital sodium-induced sleep test (PST) were used to evaluate the hypnotic effect of the SY extract. Liquid chromatography-tandem mass spectrometry and enzyme-linked immunosorbent assay were utilized to detect the levels of neurotransmitters and hormones. Molecular changes at the mRNA and protein levels were determined using real-time quantitative polymerase chain reaction and Western blot analysis to identify the mechanisms by which SY improves sleep disorders. RESULTS: The SY extract decreased sleep latency and increased sleep duration in normal mice. Similarly, the sleep duration of mice subjected to CRS was increased by administering SY. The SY extract increased the levels of tryptophan (Trp) and 5-hydroxytryptamine (5-HT) and the expression of tryptophan hydroxylase 2 (TPH2) in the cortex of normal mice. The SY extract increased the Trp level, transcription and expression of estrogen receptor beta and TPH2 in the cortex in mice with sleep disorders by decreasing the serum corticosterone level, which promoted the synthesis of 5-HT. Additionally, the SY extract enhanced the expression of arylalkylamine N-acetyltransferase, which increased the melatonin level and upregulated the expressions of melatonin receptor-2 (MT2) and Cryptochrome 1 (Cry1) in the hypothalamus of mice with sleep disorders. CONCLUSIONS: The SY extract exerted a hypnotic effect via the Trp/5-HT/melatonin pathway, which augmented the synthesis of 5-HT and melatonin and further increased the expressions of MT2 and Cry1.

Potential risk of plant viruses entering disease cycle in surface water in protected vegetable growing areas of Eastern China.

With the expansion of protected vegetable growing areas (PVGAs), viral plant diseases have become more prevalent, causing severe economic losses to the vegetable production industry in China. At present, researches on plant viruses mainly focus on plants, but there is only a few reports on the species of viruses in surface water from PVGAs. The surface water samples in PVGAs are representative to a certain extent, which has an important reference value for studying the characteristics of plant viruses in surface water. The purpose of this study was to identify the diversity and the possibility of entering disease infection cycle of plant viruses in water samples collected from PVGAs in eastern China. A total of 144 water samples were collected, and eight plant viruses including tobacco mosaic virus (TMV, 8.33%), cucumber green mottle mosaic virus (CGMMV, 33.33%), pepper mild mottle virus (PMMoV, 6.94%), cucumber mosaic virus (CMV, 0.69%), tomato masaic virus (ToMV, 3.47%), tomato mottle mosaic virus (ToMMV, 0.69%), tomato chlorosis virus (ToCV, 4.17%), and tomato yellow leaf curl virus (TYLCV, 5.56%) were examined using RT-PCR and PCR. The species of viruses in surface water varied greatly by location. CGMMV, TMV, ToCV, ToMV, ToMMV, and TYLCV were identified in Shandong, a northern part of Eastern China, whereas only PMMoV was found in Shanghai, a southern part of Eastern China. After healthy tobacco plants were inoculated with the concentrated solutions of TMV, ToMV, CGMMV, and PMMoV, could cause disease in healthy tobacco, indicating that the plant viruses in the concentrated solution have the infectivity, and the plant viruses in surface water have the possibility of entering the infection cycle of disease. The results will improve the understanding of the potential risks of waterborne disease transmission.

Antagonism of tomato spotted wilt virus against tomato yellow leaf curl virus in Nicotiana benthamiana detected by transcriptome analysis.

BACKGROUND: Tomato spot wilt virus (TSWV) and tomato yellow leaf curl virus (TYLCV) are highly harmful viruses in agricultural production, which can cause serious economic losses to crops and even devastating consequences for vegetable yield in some countries and regions. Although the two viruses belong to different families and have different transmission vectors, they share most hosts. OBJECTIVE: This study aimed to examine the transcriptomic expression of single and mixed inoculations of TSWV and TYLCV, leading to antagonism using high-throughput RNA sequencing. METHODS: We confirmed the single and mixed infections of these viruses in Nicotiana benthamiana (N. benthamiana) by artificial inoculation. And the expression changes of related genes and their biological functions and pathways during the mixed infection of TSWV and TYLCV were analyzed by comparative transcriptome. RESULTS: Basically, similar symptoms were observed in the plants singly infected with TSWV and co-infected with TYLCV; the symptoms of TYLCV in the co-infected plants were not obvious compared with single TYLCV infections. When inoculated with TYLCV, the accumulation of the virus significantly reduced in single and mixed infections with TSWV; the TSWV accumulated slightly less in co-infection with TYLCV, whereas this reduction was much smaller than that of TYLCV. The results suggested that TSWV had an antagonistic effect on the accumulation of TYLCV in N. benthamiana. It mainly focused on the changes in unique differentially expressed genes (DEGs) caused by the co-infection of TSWV and TYLCV. The eight pathways enriched by upregulated DEGs mainly included amino acid biosynthesis, citrate cycle (or tricarboxylic acid cycle, TCA cycle), and so on. However, only pentose phosphate pathway (PPP) and peptidoglycan biosynthesis could be downregulated in the Kyoto Encyclopedia of Genes and Genomes pathway in which peptidoglycan biosynthesis was involved in upregulated and downregulated pathways. CONCLUSIONS: The antagonistic effect of TSWV on TYLCV in N.benthamiana and the change trends and specific pathways of DEGs in this process were found. Our study provided new insights into the host regulation and competition between viruses in response to TSWV and TYLCV mixed infection.

CARARIME: Interactive web server for comprehensive analysis of renal allograft rejection in immune microenvironment.

Background: Renal transplantation is a very effective treatment for renal failure patients following kidney transplant. However, the clinical benefit is restricted by the high incidence of organ rejection. Therefore, there exists a wealth of literature regarding the mechanism of renal transplant rejection, including a large library of expression data. In recent years, research has shown the immune microenvironment to play an important role in renal transplant rejection. Nephrology web analysis tools currently exist to address chronic nephropathy, renal tumors and children's kidneys, but no such tool exists that analyses the impact of immune microenvironment in renal transplantation rejection. Methods: To fill this gap, we have developed a web page analysis tool called Comprehensive Analysis of Renal Allograft Rerejction in Immune Microenvironment (CARARIME). Results: CARARIME analyzes the gene expression and immune microenvironment of published renal transplant rejection cohorts, including differential analysis (gene expression and immune cells), prognosis analysis (logistics regression, Univariable Cox Regression and Kaplan Meier), correlation analysis, enrichment analysis (GSEA and ssGSEA), and ROC analysis. Conclusions: Using this tool, researchers can easily analyze the immune microenvironment in the context of renal transplant rejection by clicking on the available options, helping to further the development of approaches to renal transplant rejection in the immune microenvironment field. CARARIME can be found in http://www.cararime.com.

Efficacy Evaluation of Neoadjuvant Chemotherapy in Breast Cancer by MRI.

Breast cancer is a highly harmful malignancy, which often causes great distress to patients and seriously affects their physical and mental health. Breast cancer causes patients to experience decreased appetite, decreased eating, and indigestion, which in turn leads to malnutrition, body wasting, resistance, immune compromise, progressive anemia, cachexia, and, as a result, severe secondary infections. To investigate the efficacy evaluation of neoadjuvant chemotherapy in breast cancer by MRI, forty-eight subjects treated at the hospital from June 2014 to August 2019 were recruited. After the neoadjuvant chemotherapy, the patients were divided into two groups based on the results of histopathological examination, namely, the ineffective group (n = 14) and the effective group (n = 34). Changes in MRI indicators were compared between the two groups before and after the neoadjuvant chemotherapy. The maximum diameter of lesions decreased significantly after the neoadjuvant chemotherapy than before. The apparent diffusion coefficient (ADC) increased considerably, and the time-intensity curve (TIC) showed a transition from type III to type II/I and from type II to type I. MRI can indicate the maximum diameter of the breast cancer lesion, ADC, and TIC type. Therefore, it can be used to evaluate the efficacy of neoadjuvant chemotherapy for breast cancer and be widely applied in clinical practice.

Prediction of Tumor Mutation Load in Colorectal Cancer Histopathological Images Based on Deep Learning.

Colorectal cancer (CRC) is one of the most prevalent malignancies, and immunotherapy can be applied to CRC patients of all ages, while its efficacy is uncertain. Tumor mutational burden (TMB) is important for predicting the effect of immunotherapy. Currently, whole-exome sequencing (WES) is a standard method to measure TMB, but it is costly and inefficient. Therefore, it is urgent to explore a method to assess TMB without WES to improve immunotherapy outcomes. In this study, we propose a deep learning method, DeepHE, based on the Residual Network (ResNet) model. On images of tissue, DeepHE can efficiently identify and analyze characteristics of tumor cells in CRC to predict the TMB. In our study, we used ×40 magnification images and grouped them by patients followed by thresholding at the 10th and 20th quantiles, which significantly improves the performance. Also, our model is superior compared with multiple models. In summary, deep learning methods can explore the association between histopathological images and genetic mutations, which will contribute to the precise treatment of CRC patients.

lncRNA USP30-AS1 sponges miR-765 and modulates the progression of colon cancer.

BACKGROUND: The incidence and mortality of colon cancer is increasing recently. It is necessary to identify effective biomarkers for the progression and prognosis of colon cancer. To assess the potential of lncRNA USP30-AS1 (USP30-AS1) in serving as the biomarker of colon cancer and unearth the underlying mechanism. METHODS: There were 123 colon cancer patients enrolled. The expression of USP30-AS1 was evaluated with PCR in tissue and cell samples. The clinical significance of USP30-AS1 was assessed with a series of statistical methods, while the CCK8 and Transwell assay were conducted to estimate its biological effect on the colon cancer cellular processes. In mechanism, the interaction of USP30-AS1 with miR-765 was evaluated with the dual-luciferase reporter assay. RESULTS: In colon cancer tissues, the USP30-AS1 downregulation and the miR-765 upregulation were observed, and there was a negative correlation between the USP30-AS1 expression level and the miR-765 expression level. The downregulation of USP30-AS1 related to the malignant progression and served as an adverse prognostic indicator of colon cancer. The overexpression of USP30-AS1 dramatically suppressed colon cancer cellular processes, which was alleviated by miR-765. CONCLUSIONS: USP30-AS1 predicts the malignancy and prognosis of colon cancer patients. USP30-AS1 suppressed the progression of colon cancer through modulating miR-765.

Clinical Outcome of Free Vascularized Fibula Graft for Nonunion of Garden IV Femoral Neck Fracture of 13 Years Duration: A Case Report.

BACKGROUND: Femoral neck fractures in young patients are mostly caused by high-energy trauma and demonstrate more displacement and vertical fracture surfaces, which increase nonunion and osteonecrosis risks. Free vascularized fibula graft (FVFG) is effective in treating old femoral neck fractures and nonunion; however, available data are limited to patients within 2 years after injury or revision surgery. We present the case of a patient who was diagnosed with femoral neck fracture at the age 9 and treated with FVFG 13 years later. CASE PRESENTATION: A 9-year-old Asian girl who experienced left hip pain after an injury was diagnosed with Garden IV left femoral neck fracture, which was treated through manipulation reduction and fixed with splints. At age 16, the pain worsened after another injury and was considered to be in the physical development stage. She refused surgical treatment; hence, the fracture was fixed externally with splints. At age 22, she was hospitalized owing to a 12-day left hip pain with restricted movement caused by a fall. She was diagnosed with old Garden IV femoral neck fracture nonunion and treated with FVFG. Seven years postoperatively, imaging showed that the left femoral neck was internally fixed, the fracture had healed, and the Harris score was 90 points. The 36-Item Short Form Health Survey responses revealed that the patient's physiological functioning, emotional well-being, energy, and mental health were normal. She achieved satisfactory functional results and resumed her normal daily life. CONCLUSION: FVFG could provide satisfactory outcomes for long-term old femoral neck fractures.

Bone marrow derived mesenchymal stem cells pretreated with erythropoietin accelerate the repair of acute kidney injury.

BACKGROUND: Mesenchymal stem cells (MSCs) represent a promising treatment option for acute kidney injury (AKI). The main drawbacks of MSCs therapy, including the lack of specific homing after systemic infusion and early cell death in the inflammatory microenvironment, directly affect the therapeutic efficacy of MSCs. Erythropoietin (EPO)-preconditioning of MSCs promotes their therapeutic effect, however, the underlying mechanism remains unknown. In this study, we sought to investigate the efficacy and mechanism of EPO in bone marrow derived mesenchymal stem cells (BMSCs) for AKI treatment. RESULTS: We found that incubation of BMSCs with ischemia/reperfusion(I/R)-induced AKI kidney homogenate supernatant (KHS) caused apoptosis in BMSCs, which was decreased by EPO pretreatment, indicating that EPO protected the cells from apoptosis. Further, we showed that EPO up-regulated silent information regulator 1 (SIRT1) and Bcl-2 expression and down-regulated p53 expression. This effect was partially reversed by SIRT1 siRNA intervention. The anti-apoptotic effect of EPO in pretreated BMSCs may be mediated through the SIRT1 pathway. In a rat AKI model, 24 h after intravenous infusion, GFP-BMSCs were predominantly located in the lungs. However, EPO pretreatment reduced the lung entrapment of BMSCs and increased their distribution in the target organs. AKI rats infused with EPO-BMSCs had significantly lower levels of serum IL-1ß and TNF-α, and a significantly higher level of IL-10 as compared to rats infused with untreated BMSCs. The administration of EPO-BMSCs after reperfusion reduced serum creatinine, blood urea nitrogen, and pathological scores in I/R-AKI rats more effectively than BMSCs treatment did. CONCLUSIONS: Our data suggest that EPO pretreatment enhances the efficacy of BMSCs to improve the renal function and pathological presentation of I/R-AKI rats.

METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation.

To investigate the mechanism of renal ischemia-reperfusion injury (IRI) via regulation of N6-methyl-adenosine (m6A) and relevant genes, IRI was induced in Sprague-Dawley rats, and urine and serum creatinine levels and tissue structure changes were observed. m6A and methyltransferase-like 3 (METTL3) protein levels were assessed via dot-blot and Western blot analyses, respectively. The hypoxia/reoxygenation (H/R) cell model was constructed using NRK-52E cells, and METTL3 protein levels were assessed. METTL3 was inhibited to observe its impact on NRK-52E cell apoptosis and m6A expression in H/R processes. Methylated RNA immunoprecipitation (MeRIP) sequencing was conducted followed by MeRIP-quantitative RT-PCR and quantitative RT-PCR validation. Our results indicated that urine and serum creatinine levels increased and that renal injury and cell apoptosis were both observed in the IRI model. In additon, m6A expression increased in the IRI model, and METTL3 protein levels significantly increased in the IRI and H/R models. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, transcription factor activating enhancer binding protein 2α (tfap2a), cytochrome P-450 1B1 (cyp1b1), and forkhead box D1 (foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development. We confirmed that foxd1 mRNA and its methylation levels contributed to IRI and H/R.

Single-cell analysis reveals immune landscape in kidneys of patients with chronic transplant rejection.

Rationale: Single-cell RNA sequencing (scRNA-seq) has provided an unbiased assessment of specific profiling of cell populations at the single-cell level. Conventional renal biopsy and bulk RNA-seq only average out the underlying differences, while the extent of chronic kidney transplant rejection (CKTR) and how it is shaped by cells and states in the kidney remain poorly characterized. Here, we analyzed cells from CKTR and matched healthy adult kidneys at single-cell resolution. Methods: High-quality transcriptomes were generated from three healthy human kidneys and two CKTR biopsies. Unsupervised clustering analysis of biopsy specimens was performed to identify fifteen distinct cell types, including major immune cells, renal cells and a few types of stromal cells. Single-sample gene set enrichment (ssGSEA) algorithm was utilized to explore functional differences between cell subpopulations and between CKTR and normal cells. Results: Natural killer T (NKT) cells formed five subclasses, representing CD4+ T cells, CD8+ T cells, cytotoxic T lymphocytes (CTLs), regulatory T cells (Tregs) and natural killer cells (NKs). Memory B cells were classified into two subtypes, representing reverse immune activation. Monocytes formed a classic CD14+ group and a nonclassical CD16+ group. We identified a novel subpopulation [myofibroblasts (MyoF)] in fibroblasts, which express collagen and extracellular matrix components. The CKTR group was characterized by increased numbers of immune cells and MyoF, leading to increased renal rejection and fibrosis. Conclusions: By assessing functional differences of subtype at single-cell resolution, we discovered different subtypes that correlated with distinct functions in CKTR. This resource provides deeper insights into CKTR biology that will be helpful in the diagnosis and treatment of CKTR.

Characterization of aberrant pathways activation and immune microenviroment of BK virus associated nephropathy.

In the context of transplantation with the use of immunosuppressive drugs, BK virus infection has become the main cause of BK virus nephropathy(BKVN) in renal transplant recipients(KTRs). More importantly, BKVN may cause further allograft dysfunction and loss. However, the role of the immune microenvironment in the pathogenesis of BKVN remains unknown. Therefore, we collected microarray data of KTRs to elucidate the immune characteristics of BKVN. Via the CIBERSORT, we found that BKVN had relatively more activated memory CD4 T cells. Immunostaining showed that CD4+ and CD8+cells were significantly different between BKVN and stable allografts(STAs). In addition, the expression of immune-related genes(antigen presentation, cytotoxicity, and inflammation) was significantly higher in BKVN than in STAs. The results of gene set enrichment analysis(GSEA) and single-sample GSEA(ssGSEA) indicated that immune cell-,cytokine-,chemokine-, and inflammation-related pathways were significantly activated in BKVN, while metabolism- and renal development-related pathways were significantly downregulated in BKVN. In addition, the immune microenvironments of the peripheral blood in patients with BK viremia(BKV) or transplant kidney biopsy(TKB) with BKVN may be different. Overall, the immune microenvironment may play important roles in the occurrence and development of BKVN and provide a theoretical basis for preventing the occurrence of BKVN and finding novel treatments.

Bone mesenchymal stem cells pretreated with erythropoietin enhance the effect to ameliorate cyclosporine A-induced nephrotoxicity in rats.

An increasing number of experiments and clinical trials have demonstrated the safety, feasibility, and efficacy of mesenchymal stem cells (MSCs)-based therapies for the treatment of various diseases. The main drawbacks of MSC therapy are the lack of specific homing after systemic infusion and early death of injected cells because of the injury micro-environment. We pretreated bone mesenchymal stem cells (BMSCs) with erythropoietin (EPO) to investigate their positive effect on cyclosporine A (CsA)-induced nephrotoxicity. BMSCs were incubated with different concentrations of EPO (10, 100, 500, and 1000 IU/mL) for 24 and 48 h, and their proliferation rate, cytoskeletal morphology, migration ability, and the expression of CXCR4 were evaluated to determine the optimal pretreatment conditions. To investigate the therapeutic effects of BMSCs pretreated with EPO in CsA-induced nephrotoxicity, we established CsA-induced in vitro and in vivo toxicity models. In our in vitro study, preconditioning of BMSCs with 500 IU/mL EPO for 48 h induced a marked increase in their proliferation rate, cytoskeletal rearrangement, migration in the scrape-healing assay, and migration toward injured HK2 cells. In vivo, EPO-BMSCs showed higher ability to improve renal function than BMSCs, and in CsA-induced rats treated with EPO-BMSCs, interstitial lymphocyte infiltration, tubular swelling, necrosis, and interstitial fibrosis decreased. We demonstrated that pretreatment with 500 IU/mL EPO before infusion markedly increased the homing ability of BMSCs, and obviously ameliorate CsA-induced nephrotoxicity in rats.

[Role of miR-663 in acute renal graft rejection: an in vitro study].

OBJECTIVE: To compare the serum miR-663 levels in renal transplant patients with and without acute rejection (AR) and explore the role of miR-663 acute renal graft rejection. METHODS: Real time-PCR was used to determine serum miR-663 levels in renal transplant recipients with and without AR. MTT assay and Annexin V-FITC assay were employed to examine the viability and apoptosis of human renal glomerular endothelial cells (HRGEC) treated with a miR-663 mimic or a miR-663 inhibitor, and ELISA was performed to detect the expression of inflammation-related cytokines including IL-6, IFN-γ, CCL-2 and TNF-α in the cells. Transwell assay was used to examine the effect of miR-663 mimic and miR-663 inhibitor on the chemotactic capability of macrophages. RESULTS: Serum miR-663 level was significantly higher in renal transplant recipients with AR than in those without AR. The miR-663 mimic significantly inhibited the viability of HRGECs and increase the cell apoptosis rate, while miR-663 inhibitor suppressed the cell apoptosis. The miR-663 mimic increased the expression levels of inflammation-related cytokines and enhanced the chemotactic capability of macrophages. CONCLUSION: miR-663 might play important roles in acute renal graft rejection and may become a therapeutic target for treating AR.

Bufalin, a bioactive component of the Chinese medicine chansu, inhibits inflammation and invasion of human rheumatoid arthritis fibroblast-like synoviocytes.

Rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) contribute to the destruction of cartilage and bone by production of metalloproteinases (MMPs) into the synovial fluid and by direct invasion into extracellular matrix (ECM). Bufalin, a major component of Venenum Bufonis, can attenuate the invasion of various cancer cells. Here, we investigated the effects of bufalin on tumor necrosis factor-alpha (TNF-α)-induced invasion of RAFLSs. Western blot analysis and electrophoretic mobility shift assay were conducted to analyze the nuclear translocation of p65/nuclear factor-kappa B (NF-κB) and NF-κB DNA-binding activity. Semiquantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were performed to assess the expression of cytokines. Our results revealed that TNF-α significantly increased p65 translocation into nucleus (P < 0.01) and enhanced NF-κB DNA-binding activity, which were dose-dependently inhibited by bufalin. Furthermore, bufalin attenuated the TNF-α-induced interleukin-1beta (IL-1ß), IL-6, and IL-8 production in RAFLSs in a concentration-dependent manner. Interestingly, TNF-α-induced invasion of RAFLSs was dampened by the pretreatment of bufalin. Additionally, bufalin decreased the mRNA abundance and secretion of MMP-9 in TNF-α-treated RAFLSs. Our results reveal that bufalin can inhibit TNF-α-induced NF-κB activation, cytokine production, invasion, and MMP-9 expression in RAFLSs, indicating a therapeutic potential of bufalin on RA.

Common and unusual CT and MRI manifestations of pancreatic adenocarcinoma: a pictorial review.

Pancreatic adenocarcinoma is the most common malignancy of the pancreas with high death rate. Preoperative imaging is crucial for the assessment of the disease and the planning of treatment. In this review, we discussed the common and unusual findings of pancreatic carcinoma. The common CT and MR findings include hypovascular mass, dilataion of upstream biliary and pancreatic ducts, invasion to adjacent structures and metastasis. The uncommon CT and MR findings include: a cystic mass, a mass without dilataion of upstream ducts, multiple masses or a lesion diffusively infiltrating most parts of the pancreas without distorting its configuration.

Down-regulation of miR-200b-3p by low p73 contributes to the androgen-independence of prostate cancer cells.

BACKGROUND: An increasing body of evidence indicates that microRNAs play critical roles in androgen-independent prostate cancer (AIPC) growth. However, the regulation of the expression of microRNAs in AIPC is not very clear. In this study, we investigated the role that the interaction between miR-200b-3p and p73 plays in the proliferation of AIPC. METHODS: We compared several relevant microRNAs and cancer related genes between the androgen-dependent prostate cancer (ADPC) cell line and the AIPC cell line using quantitative real-time PCR (Q-PCR) and Western blot. Then we examined the effect of p73 and miR-200b-3p on the proliferation of AIPC and ADPC using CCK-8. Furthermore we investigated the regulation of miR-200b-3p by p73. RESULTS: p73 and miR-200b-3p were both downregulated in the PC3 cell line (AIPC). Down-regulation of both p73 and miR-200b-3p increased the proliferation of ADPC cells cultured with androgen-free medium, while up-regulation of p73 and miR-200b-3p decreased the proliferation of AIPC cells. When p73 was over-expressed in the AIPC cell subline, miR-200b-3p expression increased accordingly, while p73 was inhibited in ADPC cells cultured with androgen-free medium and miR-200b-3p expression decreased significantly. CONCLUSION: miR-200b-3p is down-regulated by low expression of p73 in AIPC cells, and this interaction contributes to the proliferation of AIPC.