Clear cell renal carcinoma (ccRCC) is the most common type of kidney cancer. CORO6 functions as an oncogene in various malignancies, including ccRCC, but the mechanisms regulating its expression, particularly at the post-translational level, remain poorly understood. Ubiquitin-specific proteases (USPs), the largest subfamily of deubiquitinases (DUBs), modulate the ubiquitination of target proteins and play crucial roles in numerous biological processes, such as ccRCC tumorigenesis. In this study, we screened USPs that potentially regulate CORO6 stability and identified USP52 as a key regulator that upregulates CORO6 expression. Bioinformatic analysis revealed that USP52 is overexpressed in ccRCC tissues and is negatively associated with patient prognosis. Similarly, USP52 expression was elevated in ccRCC cell lines, and its knockdown led to decreased CORO6 expression in these cells. In vitro experiments demonstrated that USP52 depletion reduced cell viability and proliferation, induced cell cycle arrest, increased apoptosis, and suppressed the migration and invasion of ccRCC cells. USP52 overexpression promotes the malignant phenotype of ccRCC cells. Mechanistically, USP52 interacts with CORO6, significantly decreasing its K48 ubiquitination and preventing its degradation in ccRCC cells. Notably, overexpression of CORO6 in USP52-deficient ccRCC cells effectively restored their malignant behaviors. Furthermore, using a xenograft mouse model of ccRCC, we found that USP52 deficiency impaired tumor growth in vivo, while CORO6 overexpression rescued the growth of USP52-deficient ccRCC cells. Collectively, these findings reveal that USP52 functions as an oncogene in ccRCC by deubiquitinating and stabilizing CORO6.

Vitexin, a natural flavonoid compound, has shown anti-tumor effects, but its mechanism in Renal cell carcinoma (RCC) remains unclear. Galectin-1, a β-galactoside-binding lectin, promotes tumor progression through metabolic reprogramming. This study examined whether vitexin has antitumor activity against RCC by targeting Galectin-1 and its downstream metabolic pathways. Human RCC cell lines (A498 and ACHN) were treated with vitexin to assess cell viability, apoptosis, cell cycle, migration, and invasion. Galectin-1 expression was manipulated through overexpression and knockdown approaches. Transcriptomic and metabolomic profiling were performed to identify pathway alterations. Glycolytic metabolism was evaluated using ATP measurements, glucose consumption, lactate production assays. The in vivo efficacy was validated using A498 xenograft models in nude mice. Vitexin inhibited RCC cell proliferation, while significantly downregulating Galectin-1 expression. Furthermore, vitexin treatment caused cell cycle arrest, promoted apoptosis, and suppressed colony formation, migration, and invasion. Galectin-1 overexpression rescued vitexin-induced growth inhibition and reduced apoptosis. Transcriptomic analysis revealed that Galectin-1 modulation affected PI3K-AKT pathways, with significant alterations in glycolytic genes (SLC2A1, HK1, HK2, PFKM, PFKP, LDHB). Metabolomic profiling showed Galectin-1-dependent reprogramming of oxidative phosphorylation and energy metabolism. In addition, galectin-1 knockdown impaired glycolytic flux, reduced ATP production, glucose consumption, and lactate secretion. Conversely, Galectin-1 overexpression enhanced these metabolic parameters and activated PI3K/AKT signaling, counteracting vitexin’s metabolic suppression. In vivo, vitexin significantly inhibited tumor growth, downregulated Galectin-1 and PI3K/AKT signaling, reduced cell proliferation, and increased TUNEL-positive apoptotic cells. Vitexin exerts anti-tumor effects in RCC by targeting Galectin-1, which disrupts glycolytic metabolism through PI3K/AKT signaling inhibition. These findings suggest that the vitexin targeting Galectin-1 represents a potential therapeutic strategy for treating RCC.

Abstract Although long noncoding RNAs (lncRNAs) have been implicated in the progression of prostate cancer (PCa), the functional roles of many of these molecules, especially in metastasis, remain poorly understood. To identify novel lncRNAs linked to PCa malignant phenotypes, we analyzed the differences in lncRNA expression between the highly metastatic PCa cell line (PC-3 M-1E8) and the poorly metastatic PCa cell line (PC-3 M-2B4) using transcriptome sequencing. This differential expression was confirmed by RT-qPCR, which showed that the lnc-ALX1-2 gene cluster (including lnc-ALX1-2:5, lnc-ALX1-2:7, lnc-ALX1-2:10) was significantly upregulated in PC-3 M-1E8 cells. Functional studies demonstrated that knockdown of the lnc-ALX1-2 gene cluster suppressed proliferation, migration, and invasion in PC-3 M-1E8 cells, with lnc-ALX1-2:10 showing the most prominent effect. Transcriptome analysis further revealed that lnc-ALX1-2:10 knockdown altered the expression of 194 genes related to both proliferation and migration. RT-qPCR and Western blot validated that lnc-ALX1-2:10 knockdown downregulated pro-tumorigenic factors (CCNE1, PDGFRA, ANGPT4) and EMT markers (N-cadherin, Snail, Vimentin), while upregulating ITGAL and E-cadherin. In vivo, lnc-ALX1-2:10 knockdown obviously decreased tumor volume but had no effect on mouse body weight, and molecular analysis of xenograft tumors confirmed consistent expression changes of key proteins as in vitro. Collectively, our findings identify lnc-ALX1-2:10 as a novel lncRNA that promotes aggressive phenotypes in PCa, highlighting its potential as a therapeutic target for metastatic disease.

Clear cell renal cell carcinoma (ccRCC), the most common and aggressive subtype of kidney cancer, exhibits strong metastatic potential. Alternative splicing (AS) represents a critical regulatory layer of gene expression, yet its dysregulation in ccRCC remains insufficiently characterized. ccRCC datasets from GEO were analyzed using DESeq2 for differential gene expression and AS profiling. Gene Ontology enrichment was performed for differentially expressed genes (DEGs) and differentially AS event genes (DASEGs). Findings were compared with TCGA-KIRC to identify shared and Chinese-specific DASEs. An expression regulatory network linking differentially expressed RNA-binding proteins (RBPs) to DASEGs was constructed to screen key AS-regulated genes. Functional roles of the candidate gene TLN1 were validated by molecular and cellular experiments. Analysis of GSE126964 identified 2,295 DEGs and 1,331 DASEs, both enriched in platelet activation and degranulation pathways. Intersecting DEGs and DASEGs yielded 153 key genes. Comparison with TCGA-KIRC revealed 281 Chinese-specific DASEGs, including ALDOA, TLN1, LAMP2, and CD63. The RBP–DASEG network highlighted ALDOA, TLN1, and LAMP2 as potential core regulators associated with platelet pathways. TLN1 was markedly overexpressed in ccRCC tissues and cell lines, and its knockdown significantly reduced proliferation, migration, and colony formation in vitro, supporting a pro-tumorigenic function. This study uncovers platelet-related AS dysregulation in ccRCC and identifies TLN1 as a promising biomarker and therapeutic target, offering new insights into ccRCC pathogenesis and treatment strategies.

BACKGROUND:In recent years, many studies have illustrated that the neutrophil-to-lymphocyte ratio (NLR) is a prognostic factor of metastatic castration-resistant prostate cancer (mCRPC), but their conclusions are controversial. The aim of this study was to assess the prognostic value of the NLR in patients with mCRPC treated with docetaxel-based chemotherapy. METHODS:Database searches were conducted in PubMed, EMBASE and the Cochrane Library to retrieve relevant published English-language literature up to 20 February 2023. RevMan 5.4.1 was used to summarize the hazard ratio (HR) and its 95% confidence interval (CI) for overall survival (OS) and progression-free survival (PFS) with subgroup analysis. Finally, Stata software was adopted for sensitivity analysis, and Egger's test was used to calculate the results of stability to determine whether there was publication bias. RESULTS:A total of 1,983 mCRPC patients from 14 retrospective cohort studies were included in this meta-analysis. The combined results showed that elevated NLR was significantly associated with worse OS (HR = 1.86, 95% CI: 1.55-2.23, P < 0.00001) and PFS (HR = 1.96 (95% CI: 1.52-2.53), P < 0.00001) in patients with mCRPC treated with docetaxel-based therapy. For subgroup analysis of high NLR, studies performed in Asia and cutoff value > 3 were associated with poorer OS, while cutoff values > 3 were associated with poorer PFS. CONCLUSION:Our results suggest that the neutrophil-to-lymphocyte ratio may be a prognostic factor in patients with mCPRC with docetaxel-based chemotherapy.

BackgroundOsteomyelitis is characterized by an inflammatory process initiated by microorganisms, leading to infection and subsequent degradation of bone tissue. Several studies have indicated a potential link between gut microbiota and the occurrence of osteomyelitis. Utilizing the benefits of Mendelian randomization, which mitigates issues of confounding and reverse causation, we employed this approach to ascertain the presence of a causal connection between gut microbiota and osteomyelitis. Additionally, we aimed to pinpoint gut microbiota that could potentially exert substantial influence.MethodsWe performed a rigorous screening of single nucleotide polymorphisms in GWAS summary statistics for gut microbiota and osteomyelitis. The 2,542 instrumental variables obtained after screening were subjected to MR analyses, including inverse variance weighting, weighted median, weighted mode, MR-Egger, and Mendelian randomization pleiotropy residual sum and outlier test. We then validated the reliability of the results by performing sensitivity analyses on the MR of 196 well-defined gut microbiota.ResultWe established a causal relationship between gut microbiota and osteomyelitis through MR analysis. Additionally, we identified a taxon of significant importance and six taxons with nominal significance. Specifically, the family Bacteroidales S24.7 group exhibited an association with a diminished risk of osteomyelitis development. Conversely, the class Bacilli, class Bacteroidia, order Bacteroidales, order Lactobacillales, family Streptococcaceae, and genus Coprococcus3 displayed an increased risk of developing osteomyelitis. The MR outcomes for these seven taxa remained stable throughout a series of sensitivity analyses.ConclusionThis study demonstrated a causal relationship between gut microbiota and osteomyelitis by Mendelian randomization. We hope that this study will provide a new direction for the treatment of osteomyelitis, which has a paucity of therapeutic options.

Erectile dysfunction ranks among the prevalent sexual disorders in men. Several studies have indicated a potential link between gut microbiota and erectile dysfunction. To validate this potential association, we were to screen statistical data from genome-wide association studies of gut microbiota and erectile dysfunction. p values of less than 1 × 10−5 were set as the threshold for screening instrumental variables that were strongly associated with gut microbiota. At the same time, in order to obtain more convincing findings, we further excluded instrumental variables with possible chain imbalance, instrumental variables with the presence of palindromes, instrumental variables with F-statistics less than 10, and instrumental variables associated with risk factors for erectile dysfunction. Five methods including inverse-variance weighted method, weighted median method, weighted mode, Mendelian randomization egger method and Mendelian randomization pleiotropy residual sum and outlier test were then used to analyse the 2591 instrumental variables obtained from the screening. We identified correlations between six gut microbiota and the risk of erectile dysfunction. The genus Ruminococcaceae UCG-013 exhibited an inverse association with the risk of developing erectile dysfunction (0.79 (0.65–0.97), P = 0.0214). Conversely, the genus Tyzzerella3 (1.13 (1.02–1.26), P = 0.0225), genus Erysipelotrichaceae UCG-003 (1.18 (1.01–1.38), P = 0.0412), genus LachnospiraceaeNC2004group (1.19 (1.03–1.37), P = 0.0191), genus Oscillibacter (1.23 (1.08–1.41), P = 0.0022), and family Lachnospiraceae (1.26 (1.05–1.52), P = 0.0123) demonstrated positive associations with an increased risk of erectile dysfunction. These sensitivity analyses of the gut microbiota were consistent. This study demonstrated a possible causal relationship between gut microbiota and erectile dysfunction risk through Mendelian randomization analysis, providing new potential possibilities for the prevention and treatment of erectile dysfunction.

Erectile dysfunction is a common sexual disorder in men. Some studies have found a strong association between some serum metabolites and erectile dysfunction. To investigate this association further, we used bidirectional Mendelian randomisation to investigate causality and possible biological mechanisms.Firstly, this study screened the statistics of genome-wide association studies of serum metabolites and erectile dysfunction to obtain instrumental variables. Inverse variance weighting was used as the primary method for causal effect analysis of instrumental variables in forward or reverse Mendelian randomisation, and the results obtained by MR-Egger regression and the weighted median method were used as references. Subsequently, the metabolites causally associated with erectile dysfunction were subjected to replication analyses and meta-analyses, and the results of the meta-analyses were analysed by pathway analyses to find influential pathways. In this process, Mendelian randomisation results need to be assessed for stability and reliability using sensitivity analysis.It was found that a total of six serum metabolites were causally associated with erectile dysfunction in a forward Mendelian randomisation study. 1,3,7-trimethyluraten (0.85 (0.73-0.99), P = 0.0368), ergothioneine (0.65 (0.45-0.94), P = 0.0226) and gamma-glutamylglutamate (0.63 (0.46-0.88), P = 0.0059) were protective against the development of erectile dysfunction, whereas 2-hydroxyhippurate (1.10 (1.02-1.19), P = 0.0152), N2,N2-dimethylguanosine (1.57 (1.02-2.40), P = 0.0395) and octanoylcarnitine (1.38 (1.06-1.82), P = 0.0183) were able to induce the development of erectile dysfunction. In addition, metabolic pathway analysis showed that 1,3,7-trimethylurate was able to influence the development of erectile dysfunction via the caffeine metabolism pathway (P = 0.0454). On the other hand, reverse Mendelian randomisation analysis showed that erectile dysfunction reduced serum homocitrulline levels (0.99 (0.97-1.00), P = 0.0360). Sensitivity analyses, including heterogeneity tests and pleiotropy tests, confirmed the reliability of the results.In conclusion, this study demonstrated a bidirectional causal relationship between serum metabolites and erectile dysfunction using bidirectional Mendelian randomisation analysis and replication meta-analysis. On this basis, this study provides a new direction of thinking and strong evidence for the therapeutic application and adjunctive diagnosis of serum metabolites in erectile dysfunction, and provides a certain reference value for subsequent related studies.

Abstract Objectives Bladder cancer (BCa) is one of the most frequently diagnosed cancers of the urinary tract and has a high mortality. The M2 splice isoform of pyruvate kinase (PKM2) is a key regulator of the Warburg effect in cancer cells. This study aimed to evaluate metabolic alterations and biological behaviours after knocking down PKM2. Methods In this study, 36 pairs of BCa tissues and adjacent normal tissues were collected to analyse the expression level of PKM2 and to explore the relationship between PKM2 level and tumour and patient status. After PKM2 knockdown in T24 cells, cell survival, migration, invasion, glucose uptake, lactate production, and apoptosis were detected. The tumour-forming ability of PKM2-reducing T24 cells was examined in vivo. Results The results showed that PKM2 expression correlates with BCa stage and grade. PKM2 knockdown decreases glucose consumption and lactate production and suppresses cell proliferation, migration, and invasion while increasing reactive oxygen species levels and apoptosis in T24 BCa cells in vitro. In nude mouse models, PKM2 knockdown reduced xenograft and orthotopic tumour size. Moreover, PKM2 knockdown decreased vimentin and fibronectin expression and increased E-cadherin expression. Analysis of high-throughput sequencing data revealed that PKM2 may also be associated with biological processes and diseases. Conclusions Overall, these results indicate that PKM2 may be a therapeutic target for BCa patients.

汇报1例肾血管平滑肌脂肪瘤(renal angiomyolipoma,RAML)伴静脉瘤栓年轻女性患者的诊断与治疗,并复习文献,重点探讨预防瘤栓脱落方法及保留肾单位手术的可行性.该患者尝试行机器人辅助腹腔镜下静脉取栓术+肾部分切除术,因取净瘤栓困难,血流阻断时间过长改行肾切除术.病理证实为RAML伴静脉瘤栓.RAML合并静脉瘤栓具有潜在的瘤栓脱落、肺动脉栓塞等高死亡风险.术前腔静脉滤器置入联合肾动脉栓塞可以尽可能地降低瘤栓脱落风险.保留肾单位治疗的手术方式具有挑战性,但是已经有成功案例,值得尝试.

∼30% of clear cell renal cell carcinoma (ccRCC) patients present with metastatic disease at the time of diagnosis, causing a dire 5-year survival rate of 13%. Although anti-PD-1 immunotherapy has improved survival, a strong need remains for new therapeutic options. Using integrated network analysis, we identified the mitotic regulator NDC80 as a predictor of ccRCC progression. Overexpression of NDC80 fosters the malignant phenotype by promoting cell cycle progression through S phase as well as boosting glycolysis and mitochondrial respiration. Despite high levels of immune infiltration, particularly derived from tumor resident CD8+T cells with an exhausted phenotype, NDC80 defines a class of ccRCCs that poorly respond to immune checkpoint blockade. Instead, bioinformatics identified NDC80-high ccRCCs as sensitive to inhibitors of mitotic kinases, PLK1 and AURK, therapeutic approaches we validated in cell lines and mouse xenograft studies. Thus, NDC80 status pinpoints mitotic kinase inhibitors as promising therapeutic options in difficult-to-treat ccRCCs.

Background Recent studies have suggested a possible association between gut microbiota and bipolar disorder (BD). However, observational studies are limited and there are variations between the gut microbiota taxa found in different studies. Therefore, we aimed to explore whether there is a causal relationship between gut microbiota and bipolar disorder at the genetic level and to reveal trends in the effect of influential gut microbiota on the development of bipolar disorder. Methods We conducted a Mendelian randomisation (MR) study of summary statistics from a genome-wide association study (GWAS) of gut microbiota and bipolar disorder. Inverse variance weighting (IVW) was used as the primary method of statistical analysis, while results from the MR-Egger method, weighted median, weighted mode, and MR multiplicity residuals and outliers (MR-PRESSO) tests were used for additional validation.Cochrane’s Q test, MR-Egger intercept test, and MR-PRESSO global test were used to test MR results for stability and reliability. Result We identified 13 gut microbial taxa causally associated with bipolar disorder. Betaproteobacteria, Acidaminococcaceae, Eubacterium xylanophilum group, Butyricimonas, Peptococcus, Prevotella 7, Roseburia, Terrisporobacter, Burkholderiales and Desulfovibrionales increased the risk of BD, whereas Candidatus Soleaferrea, Ruminiclostridium 5 and Victivallis decreased the risk of BD. The results of the MR analysis were shown to be reliable in the sensitivity analysis. Conclusion With the MR study, we analysed the causal relationship between 196 gut microbial taxa and bipolar disorder and also identified gut microbiota associated with the risk of developing bipolar disorder. Our findings provide new biomarkers and potential therapeutic targets for the prevention and treatment of BD.

Background: Bladder cancer (BC) is the 10th most common malignancy worldwide. The high recurrence rates of BC lead to significant treatment challenges. With the development of molecular biology techniques, research has shown that gene abnormalities are closely related to the occurrence and development of BC. This study analyzed the detection results of gene mutations in the tissue samples of BC patients and explored the relationship between fibroblast growth factor receptor 3 (FGFR3) and the prognosis and recurrence of BC. Methods: This study examined 82 Chinese patients with BC. Of these patients, 34 underwent radical cystectomy (RC), and 48 underwent transurethral resection with intravesical instillation. In addition, multigene panel targeted next-generation sequencing (NGS) of the samples was performed. Results: The mutational spectra revealed that C > T was the most common base substitution. Single nucleotide polymorphism (SNP) and deletion (DEL) were the common variant types in our cohort. The top 10 mutant genes were ROS1 (37%), PIK3CA (35%), FGFR3 (34%), BRAF (34%), ERBB2 (32%), ALK (27%), RET (27%), NTRK1 (24%), MET (23%), and EGFR (18%). FGFR3 mutations were detected more frequently in non-muscle-invasive bladder cancer (stages 0a, I) patients than in muscle-invasive bladder cancer (stage II, III, and IV) patients. The top 3 altered types of FGFR3 were p.Ser249Cys, p.Tyr375Cys, and p.Arg248Cys. Conclusions: This study examined the mutated types and frequency of FGFR3 and the prognosis of Chinese BC patients with FGFR mutations. We hope that our findings will enable clinical individualization strategies for BC patients to be optimized.

Background Pan-cancer analysis is an efficient tool to obtain a panoramic view of cancer-related genes and identify their oncogenic processes, facilitating the development of new therapeutic targets. Lysine methyltransferase 2D (KMT2D), acting as a major enhancer coactivator for mammalian cells, is one of the most frequently mutated genes across various cancer types and is considered an oncogene and a rationale for epigenetic therapeutic targets. Objective This study was designed to explore the potential role of KMT2D in human cancer through a pan-cancer analysis. Methods The expression of KMT2D was assessed in normal tissues and cell lines, and pan-cancers from The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE), and Genotype-Tissue Expression (GTE) datasets were used to explore its correlation with prognosis, immune cell infiltration, tumor mutation burden, microsatellite instability, and mismatch repair. Results KMT2D expression was heterogeneous across different cancer types. Increased KMT2D indicated a worse prognosis in adrenocortical carcinoma (ACC), brain lower-grade glioma (LGG), and mesothelioma (MESO), while patients with high KMT2D expression showed better outcomes in renal clear cell carcinoma (KIRC). Moreover, KMT2D expression was positively correlated with immune cell infiltration and negative tumor mutation burden in multiple cancers. In addition, a significant correlation between KMT2D and immune checkpoint-related genes or mismatch repair genes was identified. Conclusions These findings support the hypothesis that KMT2D is not only a potential biomarker for prognosis and immunotherapy response prediction but also an essential immune regulator in human cancer.

Long non-coding RNAs (lncRNAs) have been implicated in the progression and development of many types of cancer by interacting with RNA, DNA and proteins, including DLEU7-AS1. However, the function of DLEU7-AS1 in renal cell cancer (RCC) remains unclear. In this study, two in silico prediction algorithms were used to discover the potential target of miR-26a-5p, which was determined to be a tumor suppressor gene, possibly DLEU7-AS1, through the downregulation of coronin-3 in RCC. Thus, we hypothesized that DLEU7-AS1 promotes RCC by silencing the miR-26a-5p/coronin-3 axis. To test our hypothesis, we confirmed that DLEU7-AS1 directly targets miR-26a-5p using the pmirGLO dual-luciferase reporter assay. Next, we observed that DLEU7-AS1 expression was markedly upregulated in RCC samples and inversely correlated with clinical prognosis and miR-26a-5p levels. Knockdown of DLEU7-AS1 significantly suppressed the growth and metastasis of RCC cells in vitro and attenuated tumor growth in vivo. Interestingly, exogenous expression of coronin-3 or miR-26a-5p inhibitor treatment almost completely rescued the DLEU7-AS1 knockdown-induced inhibitory effects on cell proliferation, migration and invasion. In conclusion, our data demonstrate that DLEU7-AS1 is an oncogene in RCC capable of regulating the growth and metastasis of RCC by silencing the miR-26a-5p/coronin-3 axis, suggesting that DLEU7-AS1 can be employed as a potential therapeutic target and prognostic biomarker for RCC.

Condition being studied: As a new prognostic marker of bladder cancer, De Ritis ratio has been studied in recent years, INPLASY 1 International Platform of Registered Systematic Review and Meta-analysis Protocols INPLASY PROTOCOLDe Ritis ratio is a new biomarker for predicting the prognosis of patients with bladder cancer -a meta-analysis Zhou, X 1 ; Luo, GC 2 .To cite:

Renal pelvic hemangioma is a rare benign tumor, presenting with intermittent, total, painless, gross hematuria, accompanied by low back pain, abdominal pain or other symptoms in some cases. Four cases of pyelonephric hemangioma were treated, which were misdiagnosed as malignancy before surgery. For middle-aged patients with intermittent hematuria, if the imaging data cannot rule out renal pelvic hemangioma, it is recommended to perform renoscopy, renal artery angiography or renal puncture biopsy. For patients diagnosed with renal pelvic hemangioma, either partial nephrectomy, ureteroscopic cauterization, or selective renal artery embolization can achieve good results.

Review question / Objective: The aim of this meta-analysis is to evaluate the affect of radiotherapy in patients with upper urinary tract urothelial carcinoma to the prognosis. Condition being studied: The role of radiotherapy in patients with upper tract urothelial carcinoma is controversial. At present, there is no meta-analysis to neutralize this contradiction. Information sources: We will search, with no time restrictions, the following databases for relevant English language literature: PubMed, the Cochrane Library and Embase.

Long non-coding RNAs are a diverse catalog of RNAs that have been implicated in various aspects of tumorigenesis. Emerging evidence indicates that they play crucial roles in tumor growth, disease progression, and drug resistance. However, the clinical significance of lncRNAs in tumor behavior prediction and disease prognosis as well as the underlying mechanism in renal cell carcinoma (RCC) remains elusive. By analyzing the gene expression profiles of 539 RCC patients from the TCGA cohort and 40 RCC patients from an independent cohort, we identified FAM13A-AS1, a poorly studied lncRNA, upregulated in RCC patients. Knockdown experiments revealed that FAM13A-AS1 promotes cell proliferation, migration, and invasion by interacting with miR-141-3p. FAM13A-AS1 regulates the expression of NEK6 by decoying miR-141-3p. In addition, there was a strong positive correlation between the expression of FAM13A-AS1 and NEK6 in RCC patients. In summary, our results demonstrate the oncogenic role of FAM13A-AS1 in RCC and suggest that it promotes tumorigenesis by upregulating the expression of NEK6 by competitively binding to miR-141-3p.

The platelet-lymphocyte ratio (PLR) has been assessed in some studies on renal cell carcinoma (RCC), but the results have been inconsistent. This meta-analysis aims to review and report the latest data regarding the prognostic role of the PLR in RCC patients. Articles were searched in the PubMed, EMBASE, and Cochrane Library electronic databases. Studies were filtered according to a selection strategy, and data corresponding to the index of interest were extracted. A fixed-effects model or random-effects model was selected based on heterogeneity. The sensitivity analysis was carried out by eliminating the studies one by one. Finally, funnel plots and Egger's test were used to assess publication bias, and the trim and fill method was used to assess the impact of bias on the results. In total, 15,193 patients with RCC from 44 studies were included in this meta-analysis. The pooled analysis indicated that the higher the PLR was, the poorer the prognosis for RCC patients in terms of overall survival (hazard ratio (HR) = 1.01 (95% confidence interval (CI) 1.00, 1.02), P = 0.010), cancer-special survival (CSS) (HR = 1.21 (95% CI 1.00, 1.46), P = 0.05), progression-free survival (HR = 1.44 (95% CI 1.28, 1.62), P < 0.00001), recurrence-free survival (HR = 1.73 (95% CI 1.11, 2.71), P = 0.02), disease-free survival (HR = 1.63 (95% CI 0.91, 2.94), P = 0.01) and metastasis-free survival (HR = 1.223 (95% CI 0.712, 2.099), P = 0.466). In the subgroup analysis of high PLR, targeted treatment, TKI use, nivolumab use, surgical treatment, clear cell RCC, metastasis, Asian race, and high PLR were related to poor prognosis. This study showed that a high PLR was associated with the poor prognosis of RCC patients, but more studies are needed to confirm the value of the PLR.