[Retracted] Oncogenic miR-23a-5p is associated with cellular function in RCC.

Following the publication of this article, a concerned reader drew to the Editor's attention that, for the invasion and migration assay data shown in Fig. 4 on p. 2314, three pairs of data panels were overlapping, such that data which were intended to show the results from differently performed experiments were obtained from a smaller number of original sources. Moreover, after having conducted an internal investigation, the Editorial Office also observed that some of the flow cytometric data shown in Fig. 6 were duplicated in Fig. 7. Considering the number of overlapping data panels that have been identified in this published paper, the Editor of Molecular Medicine Reports has concluded that the article should be retracted from the publication on account of a lack of confidence in the integrity of the data. Upon contacting the authors about this matter, they accepted the decision to retract this paper. The Editor apologizes to the readership for any inconvenience caused, and thanks the interested reader for drawing this matter to our attention. [Molecular Medicine Reports 16: 2309-2317, 2017; DOI: 10.3892/mmr.2017.6829].

Erratum: [Corrigendum] miR­216a­5p acts as an oncogene in renal cell carcinoma.

[This corrects the article DOI: 10.3892/etm.2018.5881.].

Erratum: [Corrigendum] miR­199b­5p serves as a tumor suppressor in renal cell carcinoma.

[This corrects the article DOI: 10.3892/etm.2018.6151.].

Laparoscopic radical nephroureterectomy in the oblique supine lithotomy integrative position for rare renal malignant perivascular epithelioid cell tumor with renal vein cancerous thrombosis: A case report and literature review.

RATIONALE: Perivascular epithelioid cell tumor (PEComa) is a mesenchymal tumor that arises from perivascular epithelioid cells and can differentiate into melanocytes and smooth muscle cells. Malignant renal perivascular epithelioid cell tumor is extremely rare. Due to the lack of specific clinical manifestations and imaging features, diagnosing PEComa depends on postoperative pathology and immunohistochemistry. Surgery is the primary treatment for malignant PEComa because the efficacy of radiotherapy and chemotherapy is uncertain. There is still a lack of unified diagnostic criteria and treatment guidelines for renal malignant PEComa, especially with vascular invasion. Hence, the treatment experience depends on a small number of cases reported worldwide. PATIENT CONCERNS: A 68-year-old woman was admitted to our hospital due to intermittent hematuria for over 8 months. The color Doppler ultrasound and computed tomography scan revealed a mass in the lower middle part of the left kidney. DIAGNOSIS: Rare renal malignant perivascular epithelioid cell tumor with renal vein cancerous thrombosis. INTERVENTIONS: A laparoscopic radical left nephroureterectomy in the oblique supine lithotomy position was performed. OUTCOMES: The operation process went smoothly, and no pulmonary embolism occurred after the operation. The final pathological diagnosis was a renal malignant perivascular epithelioid cell tumor. After a 12-month follow-up, no recurrence or metastasis was found. LESSONS: Renal malignant PEComa is an extremely rare mesenchymal tumor diagnosed mainly based on pathology. Surgery is currently the effective treatment for malignant PEComa. For the surgical treatment of malignant renal PEComa with vascular invasion, laparoscopic radical nephroureterectomy in the oblique supine lithotomy integrative position has many benefits, as exemplified by our current case.

Laparoscopic surgery combined with the double-J tube implantation for the rare cystic-solid schwannoma of seminal vesicle: A Case Report and Literature Review.

RATIONALE: Schwannoma is common in young and middle-aged people and occurs in the head, neck, posterior mediastinum, and retroperitoneal. Schwannoma, on the other hand, is a rare occurrence in the seminal vesicle. Early diagnosis and treatment are crucial since the disease can cause lower abdominal pain, nocturia, frequent urination, blood sperm, and other symptoms. There is no standard diagnostic or treatment guideline for seminal vesicle schwannomas currently. Therefore, the treatment experience relies on the few cases reported throughout the world. PATIENT CONCERNS: A 45-year-old male patient discovered that the tumor beside the right side spermatophore is bigger than 3 years ago. DIAGNOSIS: Schwannoma of seminal vesicle. INTERVENTIONS: Ureter double-J tube implantation and laparoscopic surgery for schwannoma of seminal vesicle. OUTCOMES: The operation process went smoothly. And the patient was no discomfort after half a year. CONCLUSION: Schwannoma of the seminal vesicle is very rare in the clinic, and the imaging examination was not conclusive. The diagnosis mainly depends on pathological results. Surgical resection is the best treatment method for schwannoma. In surgery for schwannoma of seminal vesicle, combined with the ureter double-J tube implantation are many benefits. This case is an excellent example of the seminal vesicle schwannomas.

Tumor suppressor miR-33b-5p regulates cellular function and acts a prognostic biomarker in RCC.

BACKGROUND: Renal cell carcinoma (RCC) is a renal parenchyma neoplasm with a 30% recurrence rate even when treated properly. MicroRNAs are noncoding small RNAs that are involved in cellular communication and may participate in cancer development. This study aimed to explore the relationship between miR-33b-5p expression and RCC progression and prognosis. METHOD: RT-qPCR, CCK-8 assay, wound scratch assay, transwell assay and flow cytometry assay were used to evaluate the expression and function of miR-33b-5p in RCC. Additionally, RCC samples and survival data from The Cancer Genome Atlas were used to analyze the prognostic functions of miR-33b-5p. RESULTS: miR-33b-5p expression in RCC tissues and cell lines (786-O, ACHN) were found to be significantly downregulated, compared with normal tissues and cell lines (P<0.001). The miR-33b-5p mimic transfected cells showed a slower proliferation rate (P<0.01), while its invasion ability decreased by 38.16% (786-O, P<0.001) and 49.19% (ACHN, P<0.05), compared with the negative control (NC). The migration ability of both RCC lines were found to be as follows: miR-33b-5p inhibitor > NC or NC inhibitor > miR-33b-5p mimic. Additionally, TCGA and RCC samples reveal that low miR-33b-5p expression is related to poor survival outcomes (univariate analysis, P=0.029; multivariate analysis, P=0.024; Kaplan-Meier survival curves, P=0.014). Target genes prediction suggests that miR-33b-5p performs its tumor-suppressive effects and prognostic role through targeting TBX15, SLC12A5, and PTGFRN. CONCLUSIONS: miR-33b-5p may function as a tumor-suppressive regulator and prognostic biomarker in RCC.

Circular RNA atlas in osteoclast differentiation with and without alendronate treatment.

BACKGROUND: Alendronate (AL) is the most widely used bisphosphonate in the treatment of osteoporosis (OP). However, the role of circular RNAs (circRNAs) in the treatment of OP with AL remains unclear. METHODS: In this study, we showed that osteoclast (OC) precursors (OPCSs) could be induced into OCs with macrophage colony-stimulating factor (MCSF) and receptor activator of nuclear factor-κB ligand (RANKL) treatment. Subsequently, the OCs were treated with AL. OC differentiation-related biomarkers including RANK, tartrate-resistant acid phosphatase (TRAP), and cathepsin K (CTSK) were analyzed with TRAP staining, quantitative real-time (qPCR), and western blotting. Differentially expressed circRNAs (DECs) were identified among the OPCS, OC, and OC + AL groups. In addition, the expression levels of 10 DECs related to OC differentiation were verified by qPCR. RESULTS: TRAP staining showed that MCSF and RANKL treatment effectively induced OPCSs to differentiate into OCs. In addition, qPCR and western blot analysis revealed that the three biomarkers of OC (RANK, TRAP, and CTSK) were expressed significantly more in the OC group than those in the OPCS group. In contrast, the mRNA and protein expression levels of these three biomarkers decreased significantly in OCs treated with AL compared with those non-treated OCs. GO analysis of the DECs in the OPCS group vs. the OC group revealed that their functions were mainly related to cell, cell part, binding, and single-organism terms. KEGG analysis of the top 20 DECs in a comparison between the OPCS and OC groups showed that genes involved in mitogen-activated protein kinase signaling were the most common. Results of functional analyses of DECs in an OC vs. OC + AL comparison were similar to those in the OPCS vs. OC comparison. Finally, qPCR showed that, in the OC + AL vs. OC group comparison, the expression levels of seven and three DECs significantly decreased and increased, respectively. CONCLUSIONS: Having successfully induced OPCSs to differentiate into OCs, we showed that AL suppresses the differentiation of OPCS into OC and that 10 DECs were involved in the regulation of this process. This indicates that these DECs might be important to the treatment of OP.

miR-625-3p promotes migration and invasion and reduces apoptosis of clear cell renal cell carcinoma.

Clear cell renal cell carcinoma (ccRCC) is a common malignancy, yet, the mechanisms underlying tumorigenesis remain unclear. Several miRNAs have been implicated in the development of RCC previously via regulation of target gene expression. As miR-625-3p has recently been identified to play a role in development of other malignancies and is reportedly upregulated in ccRCC, we sought to investigate the role of this miRNA in the progression of ccRCC. Analysis of 30 paired fresh ccRCC tissues and adjacent normal renal tissues revealed that the expression of miR-625-3p was increased in ccRCC tissues compared to normal tissues. Subsequently, in 136 formalin-fixed paraffin-embedded ccRCC tissues, the increased miR-625-3p expression was correlated with poor prognosis for ccRCC patients. The diagnostic value of miR-625-3p was identified in 50 ccRCC patients and 74 healthy controls by ROC curve. miR-625-3p was decreased in serum of ccRCC patients compared to healthy individuals. miR-625-3p could serve as a promising serum biomarker for yielding an area under the receiver operating characteristic curve of 0.792 with 70.3% sensitivity and 80.0% specificity in discriminating ccRCC from healthy individuals. Using in vitro functional assays, we found that overexpression of miR-625-3p promoted migration and invasion of ccRCC cells but reduced ccRCC cell apoptosis. Inhibition of miR-625-3p, on the other hand, exerted the opposite effects. Bioinformatic analyses indicated that predicted gene targets of miR-625-3p are correlated with lower overall survival of ccRCC patients. Together, these findings demonstrate that miR-625-3p promotes ccRCC migration and invasion and reduces apoptosis, providing a prognostic marker for survival and a potential diagnostic and therapeutic target against ccRCC.

MiR-23a-3p acts as an oncogene and potential prognostic biomarker by targeting PNRC2 in RCC.

BACKGROUND: Renal cell carcinoma (RCC) is a most common kidney malignancy, with atypical symptoms in the early stage and poor outcome in the late stage. Recently, emerging evidence revealed that some miRNAs play an essential role in the tumorigenesis and progression of RCC. Therefore, the aim of this study is that understand the detailed molecular mechanism of miR-23a-3p in RCC and identify its potential clinical value. METHODS: In this study, RT-qPCR, wound scratch assay, cell proliferation assay, transwell assay and flow cytometry assay were performed to detect miR-23a-3p expression and its proliferation, migration and apoptosis in RCC. The bioinformatics analysis, RT-qPCR, western blot and luciferase reporter assay were performed to discern and examine the relationship between miR-23a-3p and its potential targets. Moreover, we analyzed the relationship between miR-23a-3p expression and clinicopathological variables or overall survival (OS) from 118 formalin-fixed paraffin-embedded RCC samples. RESULTS: miR-23a-3p is significantly up-regulated in RCC tissue samples, RCC cell lines and the TCGA database. Upregulating miR-23a-3p enhances, while silencing miR-23a-3p suppresses cell viability, proliferation and mobility in ACHN and 786-O cell lines. Besides, overexpression of miR-23a-3p inhibits the cell apoptosis. Then our study further reveals that miR-23a-3p regulates tumorigenesis by targeting Proline-Rich Nuclear Receptor Coactivator 2 (PNRC2). Also, the cox proportional hazard regression analysis indicates that low expression of miR-23a-3p patients has a remarkable longer OS. CONCLUSIONS: Our results reveals that miR-23a-3p may not only serve as a new biomarker for prognosis but also serve as a new therapeutic strategy in the RCC treatment.

Primary small-cell neuroendocrine carcinoma of the urinary bladder: A rare case and a review of the literature.

Primary small-cell neuroendocrine carcinoma (SCNEC) of the urinary bladder is a rare tumor characterized by poor differentiation and high aggressiveness. Only ~150 cases have been reported in the literature to date. We herein present a case of an 87-year-old man who presented with hematuria and was found to have an ill-defined mass in the urinary bladder on computed tomography and cystoscopic examination. On pathological examination following tumor biopsy, the mucosa of the bladder wall was found to be extensively infiltrated by neuroendocrine carcinoma, positive for CD56 and synaptophysin and negative for epithelial membrane antigen, consistent with SCNEC of the urinary bladder. The patient refused further surgical treatment and succumbed to the disease 2 months after the diagnosis. In the present study, this rare case of primary SCNEC of the urinary bladder is presented, along with a discussion on the clinical presentation, immunohistochemical and cytomorphological characteristics, management, biological behavior and prognosis of this disease.

Oncogene miR-154-5p regulates cellular function and acts as a molecular marker with poor prognosis in renal cell carcinoma.

AIMS: In adult population, the renal cell carcinoma (RCC) is one of the most common urological malignancies. It is meaningful to research for the molecular markers which are involved in the occurrence and development of RCC. Therefore, we concentrate on illuminating the role of microRNA-154-5p in progression of RCC and explore its prognostic values. MAIN METHODS: The real-time quantitative polymerase chain reaction (RT-qPCR) was applied to determine expression level of miR-154-5p in tissues. Afterwards, the transfected cell lines ACHN and 786-O were used for the CCK-8 assay, MTT assay, wound healing assay, transwell assay and flow cytometric assay to explore the role of miR-154-5p in regulating cellular function. In addition, formalin-fixed paraffin-embedded (FFPE) renal cancer samples were used for detecting the relationship between expression level of miR-154-5p and clinical information. Furthermore, univariate and multivariate Cox proportional-hazards regression analyses, and the Kaplan-Meier survival curves were performed to evaluate the prognostic value of miR-154-5p in RCC. KEY FINDINGS: The RT-qPCR indicated that miR-154-5p is up-regulated in RCC pathologic specimens and cell lines. Results of study also demonstrated that upregulation of miR-154-5p reduced cell apoptosis and promoted cell proliferation, viability, migration as well as invasion in RCC cells. The prognosis analyses indicated that the expression level of miR-154-5p is associated with the prognosis of renal cancer, and the overall survival of patients with low expression is longer. SIGNIFICANCE: The present study revealed that the oncogene miR-154-5p regulates cellular function and acts as a molecular marker with poor prognosis in renal cell carcinoma.

Erratum: miR-199b-5p serves as a tumor suppressor in renal cell carcinoma.

[This corrects the article DOI: 10.3892/etm.2018.6151.].

MiR-302b regulates cell functions and acts as a potential biomarker to predict recurrence in bladder cancer.

BACKGROUND: Bladder cancer is the most common urogenital tumor with substantial morbidity, high recurrence rate and mortality. miRNAs, a class of endogenous noncoding RNA, were found to involve in the genesis, maintenance and metastasis of cancer. Genomic profiling revealed that miR-302b is down-regulated in bladder cancer while its functions in bladder cancer remain to be ascertained. METHODS: Cell functional assays including wound healing assay, CCK-8 assay, Transwell assay and flow cytometry assay were performed to clarify the functions of miR-302b expression in cell proliferation, migration, invasion and apoptosis in BC. Furthermore, RT-qPCR was performed to study the expression of miR-302b in bladder cancer tissues and the prognostic value of altered miR-302b expression with 48 formalin-fixed paraffin-embedded bladder urothelial carcinoma samples. RESULTS: The results of RT-qPCR demonstrated that expression level of miR-302b was significantly reduced in bladder cancer tissues and cell lines. The cells after transfected with miR-302b mimic showed lower mobility, lower proliferation and increased apoptosis, while opposite results were obtained after inhibiting the expression of miR-302b. The prognosis analysis demonstrated that the patients with low expression of miR-302b experienced high risks of recurrence. CONCLUSIONS: The results of our study demonstrate that miR-302b regulates cell functions and acts as a potential biomarker to predict recurrence in bladder cancer.

Oncogenic miR-425-5p is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma.

An increasing number of studies have demonstrated the function of microRNAs (miRNAs) in the initiation and development of various types of cancer. Among them, miR-425-5p is proven to serve an important function in several types of cancer, including gastric, cervical cancer, and hepatocellular carcinoma. However, the function of miR-425-5p in renal cell carcinoma (RCC) remains unclear. In the present study, it was demonstrated that the expression level of miR-425-5p was upregulated in RCC tissues and cell lines compared with normal tissues and cell lines (P<0.05). Additionally, Cell Counting kit-8 and MTT assays were employed to assess cell viability and proliferation, whereas wound healing and Transwell assays were employed to examine migration and invasion. The results demonstrated that upregulation of miR-425-5p promoted cell viability and the invasion and migration of ACHN and 786O cells (P<0.05). Flow cytometric analysis confirmed that upregulation of miR-425-5p inhibited apoptosis of ACHN and 786O cells (P<0.05). Downregulation of miR-425-5p inhibited the viability and invasion and migration of ACHN and 786O cells (P<0.05). In the present study, upregulation of miR-425-5p inhibited apoptosis of ACHN and 786O cells whereas no differences in early apoptotic rate were observed between the inhibitor and inhibitor NC groups for 786O and ACHN cells. These results indicate that miR-425-5p may act as an oncogene in RCC.

Oncogenic miR-663a is associated with cellular function and poor prognosis in renal cell carcinoma.

BACKGROUND: MicroRNA(miRNA) plays a key regulatory role in various stages of tumorigenesis, including cell growth, cell cycle control, apoptosis avoidance, tissue invasion, and metastasis. Several microRNAs are involved in the development of renal cell carcinoma (RCC) and the malignant transformation process. However, the effects of miR-663a on RCC have rarely been reported. METHODS: In the present study, the expression of miR-663a was examined in RCC using matched normal kidney tissues and four cell lines (786-O, Caki-1, ACHN and HK-2). MicroRNA mimics were transiently transfected into RCC cells and the effects of over expression on proliferation, migration, invasion, and apoptosis was observed. In addition, the relationship between miR-663a expression in 42 formalin-fixed paraffin-embedded (FFPE) clear cell renal carcinoma (ccRCC) samples and clinical pathological variables and overall survival was investigated. We evaluated the prognostic value of miR-663a expression in ccRCC by experimental results. RESULTS: The results showed that the expression of miR-663a was up-regulated in RCC cells and tissues and miR-663a was associated with proliferation, migration, invasion, and apoptosis of RCC. Cox proportional hazard regression analysis showed that a high expression of miR-663a patients had a significantly shorter overall survival in univariate and multivariate analysis. Kaplan-Meier survival curves showed that a high expression of miR-663a patients had a significantly shorter overall survival. CONCLUSIONS: These results indicate that miR-663a can be used as an independent marker for the poor prognosis of ccRCC, and may also play an important role as a tumor oncogene in the occurrence and development of RCC.

miR-199b-5p serves as a tumor suppressor in renal cell carcinoma.

MicroRNA (miR)-199b-5p has been reported to have a critical role in various types of malignancy. However, the exact function miR-199b-5p in renal cancer remains to be fully elucidated. The present study aimed to detect the expression levels of miR-199b-5p in renal cell carcinoma (RCC) tissues and RCC cell lines, and investigated the effect of miR-199b-5p in vitro with Cell Counting Kit-8, MTT, scratch wound, Transwell and flow cytometric assays. The results demonstrated that the expression levels of miR-199b-5p were significantly downregulated in RCC tissues and cell lines compared with those in paired adjacent normal renal tissues and a reference cell line, respectively. Downregulation of miR-199b-5p by transfection with a synthetic inhibitor promoted cellular proliferation and migration, while reducing the apoptotic rate, indicating that miR-199b-5p may serve as a tumor suppressor in RCC. Further study is required to identify target genes of miR-199b-5p to elucidate the mechanisms underlying the role of miR-199b-5p in the occurrence and development of RCC.

Oncogene miR-187-5p is associated with cellular proliferation, migration, invasion, apoptosis and an increased risk of recurrence in bladder cancer.

BACKGROUND: Bladder cancer, the ninth-most-common malignancy worldwide with an estimated 356,000 new cases and 145,000 deaths annually, has a propensity to relapse, requiring lifelong monitoring after diagnosis. 75% patients diagnosed with BC are non-muscle invasive BC and over 50% of them experience recurrences within 6-12 years of initial diagnosis. miRNA are small, noncoding RNA and shown to be oncogenes or anti-oncogenes in bladder cancer, contributing to numerous BC cell processes, including cell proliferation, differentiation, migration and apoptosis. METHODS: RT-qPCR were performed to detect the expression of miR-187-5p in tissues and cell lines, After which, clinicopathological variables and the prognostic value of altered miR-187-5p expression in BC was analyzed with the 48 formalin-fixed paraffin-embedded BC samples. Moreover, Cell functional assays (wound healing assay, CCK-8 assay, transwell assay and flow cytometry assay) were performed to explore the relationship between miR-187-5p expression and cell proliferation, migration, invasion and apoptosis in BC. RESULTS: Up-regulation of miR-187-5p was observed in BC tissues and BC cell lines. Cox proportional hazard regression analysis demonstrated that the patients with low expression of miR-187-5p experience lower risks of recurrence in the univariate and multivariate analysis. The Kaplan-Meier recurrence-free curves suggested that the patients with low expression of miR-187-5p experience lower risks of recurrence. Up-regulation of miR-187-5p promotes cell proliferation and mobility and inhibits the apoptosis of 5637 and UM-UC-3 cell, while down-regulation of miR-187-5p reverses these effects. CONCLUSIONS: The results of our study demonstrated that oncogene miR-187-5p is associated with cellular proliferation, migration, invasion, apoptosis and an increased risk of recurrence in bladder cancer.

Tumor suppressor miR-211-5p is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma.

Increasing evidence has demonstrated that microRNA (miRNA) serve an important role in the tumorigenesis of various types of cancer, such as renal cell carcinoma (RCC). The expression of miR-211-5p has been detected in RCC tissue by microarray profiling. However, studies regarding miR-211-5p and RCC remain rare. In the present study, the expression of miR-211-5p in RCC tissues and cell lines was revealed to be downregulated by reverse transcription-quantitative polymerase chain reaction analyses. The present results also revealed that the upregulation or downregulation of miR-211-5p inhibited or promoted, respectively, RCC cell proliferation, migration and invasion. In addition, the upregulation or downregulation of miR-211-5p induced or inhibited, respectively, RCC cell apoptosis. However, the present study only identified that downregulation of miR-211-5p promoted 786O and ACHN cell viability. The above results suggest that miR-211-5p may be a tumor suppressor in the tumorigenesis of RCC and may be a potential therapeutic target for RCC in the future. Further research should focus on the underlying mechanism of miR-211-5p in RCC and on investigating the possible use of miR-211-5p as a biomarker for RCC.