With the gradual improvement in tumor immunotherapy, the incidence of immune-related adverse events (irAEs) has increased. However, according to current research, the relationship between irAEs and prognosis remains a contentious issue. This study used bibliometrics research to investigate hotspots and future trends on the relationship between irAEs and prognosis and to serve as a resource for researchers in this field. In the core literature database of Web of Science, the keywords immune checkpoint inhibitors(ICIs), immune-related adverse events, prognosis were used to search for the articles and reviews in the field of irAEs and prognosis. Set the time parameter to January 2007 to December 2023. Visualization analysis software CiteSpace 6.1.R6, VOSviewer1.6.18 and Carrots2 were used to conduct quantitative statistical and visual research on the author, institution, country, keyword, publication, cited literature, research status, research hotspots and development trends of the relevant research. The analytic research was based on original articles and reviews. 724 articles from 308 countries led by China(147)，the United States(131), and Japan(105) were included. The most popular tumor type is melanoma, small-cell lung cancer, and renal cell carcinoma. The focus topics in this field encompass “Myasthenia gravis,” “neurotoxicity,” “liver damage,” “head and neck adverse events,” “colitis,” and “skin adverse events.” This study has provided a valuable reference for future research in this field. Combination therapy, predictive biomarkers, patients’ preexisting conditions, glucocorticoids, prognostic indicators, ICI rechallenge, and other topics could become research hotspots which will help us to identify useful information from complex big data and provide a basis for precise medicine for immune checkpoint inhibitor therapy.

ETHNOPHARMACOLOGICAL RELEVANCE:Cardiovascular disease (CVD) and fatigue are two common diseases endangering human life and health that may interact and reinforce one another. Myocardial infarction survivors frequently experience fatigue, and acute myocardial infarction (AMI) is one of the most common cardiovascular diseases that cause fatigue-induced sudden death. Sheng Mai Yin (SMY), a Chinese medicine prescription, is traditionally used for the treatment of diabetes and cardiovascular disease, and has been demonstrated to reduce fatigue and safeguard cardiac function.AIM OF THE STUDY:This study aims to investigate the effects and underlying mechanisms of SMY in treating fatigue and AMI.MATERIALS AND METHODS:The pharmacological mechanisms of SMY in treating fatigue and AMI were predicted by bioinformatics and network pharmacology methods. After administering SMY at high, medium and low doses, the swimming time to exhaustion, hemoglobin level, serological parameters and hypoxia tolerance time were detected in C57BL/6N mice, and the left ventricular ejection fractions (LVEF), left ventricular fractional shortening (LVFS), grasp strength, cardiac histopathology, serological parameters and the expression of PINK1 and Parkin proteins were examined in Wistar rats.RESULTS:371 core targets for SMY and 282 disease targets for fatigue and AMI were obtained using bioinformatics and network pharmacology methods. Enrichment analysis of target genes revealed that SMY might interfere with fatigue and AMI through biological processes such as mitochondrial autophagy, apoptosis, and oxidative stress. For in vivo experiments, SMY showed significant anti-fatigue and hypoxia tolerance effects in mice; It also improved the cardiac function and grasp strength, decreased their cardiac index, myocardial injury and fibrosis degree, and induced serological parameters levels and the expression of PTEN-induced putative kinase 1 (PINK1) and Parkin proteins in myocardium, suggesting that SMY may exert cardioprotective effects in a joint rat model of fatigue and AMI by inhibiting excessive mitochondrial autophagy.CONCLUSION:This study revealed the anti-fatigue, anti-hypoxia and cardioprotective effects of SMY in a joint model of fatigue-AMI, and the pharmacological mechanism may be related to the inhibition of mitochondrial autophagy in cardiomyocytes through the PINK1/Parkin pathway. The discoveries may provide new ideas for the mechanism study of traditional Chinese medicine, especially complex prescriptions, in treating fatigue and AMI.

The dysregulation of protein-coding genes involved in various biological functions is closely associated with the progression of thyroid cancer. This study aimed to investigate the effects of dysregulated gene expressions on the prognosis of classical papillary thyroid carcinoma (cPTC). Using expression profiling datasets from the Cancer Genome Atlas (TCGA) database, we performed differential expression analysis to identify differentially expressed genes (DEGs). Cox regression and Kaplan-Meier analysis were used to identify DEGs, which were used to construct a risk model to predict the prognosis of cPTC patients. Functional enrichment analysis unveiled the potential significance of co-expressed protein-encoding genes in tumors. We identified 4 DEGs (SALL3, PPBP, MYH1, and SYNDIG1), which were used to construct a risk model to predict the prognosis of cPTC patients. These 4 genes were independent of clinical parameters and could be functional in cPTC carcinogenesis. Furthermore, PPBP exhibited a strong correlation with poorer overall survival (OS) in the advanced stage of the disease. This study suggests that the 4-gene signature could be an independent prognostic biomarker to improve prognosis prediction in cPTC patients older than 46.

ObjectiveThe primary objective of this paper is to investigate the research hotspots and future trends of immune-related adverse events induced by immune checkpoint inhibitors, offering valuable insights for researchers in this field.MethodologyUsing the visual analysis software, this study conducted quantitative statistics and visualization research on the relevant literature concerning immune-related adverse events caused by immune checkpoint inhibitors in the Web of Science Core Collection Database. By evaluating the publication trends, countries, institutions, keywords, research status, cited documents, and document co-citations, among several others, the discussion revolved around the hot spots and future development trends in this field and provided references for future research.Findings and conclusionsA total of 514 English articles were included, and the top three countries in the research field at the time of this study were the United States, Japan, and China. More specifically, the University of Texas MD Anderson Cancer Center, Dana-Farber Cancer Institute, and Massachusetts General Hospital have been the top three research institutes with more than 10 publications. The frequency of keyword use linked to immune-related adverse events caused by immune checkpoint inhibitors in literature research has been steadily growing over the years. Additionally, the research with respect to the disease focuses on melanoma, cell lung cancer, hepatocellular carcinoma, and breast cancer. In the context of drugs, cancer-related research has mainly focused on the combined use of nivolumab, pembrolizumab, ipilimumab, and immune checkpoint inhibitors. Meanwhile, research on adverse events has delved into the immune checkpoint inhibitors causing vitiligo, thyroid dysfunction, pancreatitis, cholangitis, and rheumatism. Related studies cover acute arthritis, myositis, acute kidney injury, as well as the combination therapy of immune checkpoint inhibitors and docetaxel, management of irAEs in cancer immunotherapy, and biomarkers of immune adverse reactions of immune checkpoint inhibitors. Finally, case report studies of immune adverse reactions caused by immune checkpoint inhibitors could serve as research hotspots in the future.

BACKGROUND:As the tissue with the highest selenium content in the body, the occurrence and development of thyroid cancer are closely related to selenium and selenoproteins. Selenium-binding protein 1 (SBP1) has been repeatedly implicated in several cancers, but its role and molecular mechanisms in thyroid cancer remains largely undefined.METHODS:The expression of SBP1, sodium/iodide symporter (NIS) and thioredoxin (TXN) were analyzed in clinical samples and cell lines. Cell counting kit-8 (CCK-8) and tube formation assays were used to analyze the cell viability and tube formation of cells. Immunofluorescence was used to determine the expression of the NIS. Co-immunoprecipitation (Co-IP) assay was carried out to verify the interaction of SBP1 with TXN. The mouse xenograft experiment was performed to investigate the growth of thyroid cancer cells with SBP1 knockdown in vivo.RESULTS:SBP1 was significantly increased in human thyroid cancer tissues and cells, especially in anaplastic thyroid cancer. Overexpression of SBP1 promoted FTC-133 cell proliferation, and the culture supernatant of SBP1-overexpression FTC-133 cells promoted tube formation of human retinal microvascular endothelial cells. Knockdown of SBP1, however, inhibited cell proliferation and tube formation. Furthermore, overexpression of SBP1 inhibited cellular differentiation of differentiated thyroid cancer cell line FTC-133, as indicated by decreased expression of thyroid stimulating hormone receptors, thyroglobulin and NIS. Knockdown of SBP1, however, promoted differentiation of BHT101 cells, an anaplastic thyroid cancer cell line. Notably, TXN, a negative regulator of NIS, was found to be significantly upregulated in human thyroid cancer tissues, and it was positively regulated by SBP1. Co-IP assay implied a direct interaction of SBP1 with TXN. Additionally, TXN overexpression reversed the effect of SBP1 knockdown on BHT101 cell viability, tube formation and cell differentiation. An in vivo study found that knockdown of SBP1 promoted the expression of thyroid stimulating hormone receptors, thyroglobulin and NIS, as well as inhibited the growth and progression of thyroid cancer tumors.CONCLUSION:SBP1 promoted tumorigenesis and dedifferentiation of thyroid cancer through positively regulating TXN.

Background Cryptotanshinone (CPT), an active component extracted from the root of Salvia miltiorrhiza Bunge, exhibits extensive favorable bioactive properties including anti-inflammatory, antioxidative, antibacterial, and antitumor effects. This study aims to investigate the effects of CPT on osteogenesis and explore related mechanisms both in vivo and in vitro. Methods In the in vivo experiment, ovariectomized (OVX) female rats were intragastrically administered with CPT at doses of 10 mg/kg and 20 mg/kg for 13 consecutive weeks. Dual-energy X-ray absorptiometry was employed to detect bone mineral density (BMD). ELISA assay was leveraged to detect the biochemical parameters such as BUN and creatinine in the kidney samples. Bone and kidney sections were dyed by H&E and Masson staining kits. In the in vitro experiment, the RAW 264.7 cells were stimulated through the receptor activation of the nuclear factor kappa B ligand (RANKL) to establish an osteoclast differentiation model, and CPT's protective effect against bone loss was evaluated. Differentiated osteoclasts were determined by TRAP staining. While, osteoclast-marker proteins such as NFATc1, c-Fos, and cathepsin K were identified by Western blot. Results The results from in vivo experiments revealed that CPT could elevate bone mass and increase bone formation markers in OVX rats. Intriguingly, CPT administration noticeably ameliorated the kidney injury in OVX rats by suppressing BUN and restoring creatinine levels. Furthermore, the results from in vitro experiments suggested that CPT downregulated the protein expression of osteoclast-associated genes such as cathepsin K, c-Fos, and NFATc1 which hinted the related potential mechanisms. Conclusion The evidence from in vivo and in vitro experiments suggested that CPT exerted antiosteoclastogenic effects by inhibiting the activation of osteoclast differentiation followed by suppressing the protein expressions of cathepsin K, c-Fos, and NFATc1 in osteoclast precursors, and it exhibited protective effects against kidney damage, which highlighted its advantage in clinical application.

目的:对比分析经外环下精索静脉结扎术与腹股沟显微精索静脉结扎术对精索静脉曲张患者的精液质量及性激素水平的影响.方法:113例研究对象,随机分为观察组(n=57)和对照组(n=56),对照组给予腹股沟显微精索静脉结扎术,观察组给予经外环下精索静脉结扎术,对比其精液质量、性激素水平以及并发症发生率.结果:术后半年,两组患者精子密度等相关指标均显著提高,且观察组均较对照组高(P＜0.05);两组患者术后血清促卵泡激素(follicle-stimulatinghor-mone,FSH)、血清睾酮(testoster-one,T)、黄体生成素(luteinizing hormone,LH)浓度水平比较,观察组显著较对照组低(P＜0.05),术后血清T水平显著升高,观察组显著高于对照组(P＜0.05);两组患者术后2周内并发症发生情况比较,观察组低于对照组(P＜0.05).结论:相比于腹股沟显微精索静脉结扎术,经外环下精索静脉结扎术更有利于患者精子质量的提高,改善性激素水平,降低患者并发症发生率,值得推广应用.

目的:探讨围术期循证护理对动静脉内瘘狭窄经皮球囊扩张术患者的护理效果及术后并发症的影响.方法:选取我院2016年12月至2018年12月的98例经皮球囊扩张术患者进行干预研究,随机分为干预组和对照组各49例,对照组采用常规护理,干预组在对照组的基础上进行围术期循证护理,干预1个月,观察2组患者的护理效果、生活质量及并发症.结果:干预组的手术成功率(98.0％)明显高于对照组(77.6％),具有统计学意义(P<0.05);干预组的生活质量评分明显高于对照组,具有统计学意义(P<0.05);干预组的并发症发生率(2.0％)明显低于对照组(20.4％),具有统计学意义(P<0.05).结论:采用围术期循证护理对经皮球囊扩张术患者进行干预可以提高手术成功率,减少并发症发生,提高患者的生活质量.

Hyperammonemia is the excessive accumulation of ammonia in the blood, and is usually defined as a plasma level above 100 µmol/L in neonates or above 50 µmol/L in term infants, children, and adolescents. Patients with hyperammonemia usually experience life-threatening neuropsychiatric symptoms, especially newborns. It is routinely caused by inherited metabolic diseases and also by acquired disorders, such as liver failure, portosystemic shunting, gastrointestinal hemorrhage, ureterosigmoidostomy, renal tubular acidosis, hypoxic ischemic encephalopathy, infections with urea-metabolizing organisms, and some drugs. Transient hyperammonemia of the newborn (THAN) is a special type of hyperammonemia acknowledged in the field of metabolic disease as an inwell-defined or well-understood entity, which can be diagnosed only after the exclusion of genetic and acquired causes of hyperammonemia. Although the prognosis for THAN is good, timely identification and treatment are essential. Currently, THAN is underdiagnosed and much less is mentioned for early diagnosis and vigorous treatment. Herein, we present common themes that emerge from the pathogenesis, diagnosis, and management of THAN, based on current evidence. When a newborn presents with sepsis, intracranial hemorrhage, or asphyxia that cannot explain coma and seizures, doctors should always keep this disease in mind.

目的 分析预防性颈侧区淋巴结清扫对CN0期甲状腺乳头状癌(PTC)患者的临床价值.方法 回顾性分析2015年12月—2019年12月收治的784例CN0期PTC患者的临床资料.根据手术方法分为A组343例和B组441例,A组行甲状腺全切加中央区淋巴结清扫术,B组在A组基础上给予患侧预防性颈侧区淋巴结清扫术.分析2组颈部淋巴结转移情况,比较手术前后甲状旁腺功能、血钙水平、并发症及预后.结果 784例CN0期PTC患者中发生颈部淋巴结转移338例(43.11％).与术前比较,2组术后7 d甲状旁腺激素、血钙水平显著下降,且B组下降更为显著(P<0.05,P<0.01).2组术后并发症总发生率比较差异无统计学意义(P>0.05).术后随访1年,与A组比较,B组局部复发率和再次手术率均明显降低(P<0.05).结论 预防性颈侧区淋巴结清扫可降低CN0期PTC局部复发率,减少因淋巴结转移导致的再次手术.

显微外科技术的应用使男性不育症的治疗进入新的发展阶段.现阶段男性不育症治疗的主要矛盾是临床上大量患者需要得到规范的手术治疗,而专业的显微男科手术医师数量又相对不足.同时,男性生殖器官的解剖特点,如输精管与附睾管的结构又区别于普通显微外科所面对的血管和神经.因此,针对这一特殊疾病,需要对男科手术医师进行科学、规范的显微外科技术培训.是否熟练掌握男性不育显微外科技术已经成为衡量当代男科手术医师是否合格的标准之一.通过开展系统的男性不育显微外科培训,可以为各级医院培养专业的显微男科手术医师,使广大男性不育症患者得到及时、规范的治疗.

目的 探讨剪切波弹性成像在精索静脉曲张相关男性不育症诊断中的临床应用价值.方法 选取在我院就诊的精索静脉曲张患者74例(左侧精索静脉单侧曲张Sarteschi分级≥3级),根据精液质量分为精液正常组37例和弱精症组37例,另选74例健康成人为健康对照组,常规超声测量各组睾丸体积,剪切波弹性成像检测睾丸硬度,并对其结果进行比较分析.结果 精液正常组和弱精症组左侧睾丸硬度分别为(5.03±2.68)kPa、(7.23±1.88)kPa,差异有统计学意义(P=0.002);两组与健康对照组左侧睾丸硬度比较差异均有统计学意义(均P<0.001).精液正常组左侧睾丸体积为(15.85±2.6)ml,与健康对照组左侧睾丸体积比较差异无统计学意义(P=0.587);弱精症组左侧睾丸体积为(13.19±2.10)ml,与健康对照组比较差异有统计学意义(P<0.05).精液正常组左侧睾丸体积与右侧比较差异无统计学意义(P=0.813),硬度高于右侧(P<0.001);弱精症组左侧睾丸体积低于右侧,硬度高于右侧,差异均有统计学意义(均P<0.05).结论 剪切波弹性成像是评估精索静脉曲张相关男性不育症的一种有效手段,具有较好的临床应用价值.

目的 以人附睾组织为研究对象,进行附睾管三维重建,明确附睾管解剖学及组织学特点.方法 对1例人附睾连续组织切片,Leica-Aperio AT2数字扫描,Photoshop CC 2018配准,VGStudio MAX V3.0三维立体合成,Materialise Magics V22.0后期修饰.另1例用于电子显微镜观察.结合切片及三维重建,分析附睾管的组织学特点.结果 获得7 μm厚的横断面人附睾石蜡切片4331张,矢状面切片543张;人附睾管存在明显的区域性分布,附睾头、体和尾部可分别划分为7个、9个和4个亚区,亚区间有组织间隔;不同亚区内附睾管排列无序,但附睾管管径及其上皮结构存在差异,且体、尾部各亚区间为单根附睾管连接.结论 利用连续组织切片的方法能成功三维重建人附睾管.揭示人附睾管具有明显的空间区域性,不同亚区组织存在差异.

医学生实习阶段的学习是医学生能否成为优秀医生的关键时期.围绕培养具有扎实理论知识,较强实践技能及较高综合素质这一医学教学目标,有很多教改及教学手段,但不能全面涵盖上述目标.通过指定实习医学生以所管疾病为讲课内容,指导学生复习所学专业基础知识,检索该疾病的研究新进展,这不仅培养了实习学生的扎实理论知识,还训练了学生的语言组织、表达能力,逻辑思维能力和沟通能力,能有效改善医学生的综合素质.

目的 了解北京市西城区三甲医院护理人员组织支持感、职业倦怠与抑郁倾向现状并分析其相关性.方法 2019年7-12月运用随机抽样方法,选取北京市3家市级三级甲等医院503名正式在职护理人员作为研究对象,运用组织支持感量表、职业倦怠量表、流调用抑郁自评量表对护理人员进行调查和分析.结果 不同科室、性别、婚姻状况的护理人员组织支持感、职业倦怠及抑郁倾向的得分差异均无统计学意义(均P＞0.05).儿科护理人员的抑郁倾向得分最高(19.09±10.71),女性护理人员的抑郁倾向得分(18.21±11.47)高于男性护理人员(17.87±11.54);未婚护理人员抑郁倾向得分(18.84±12.44)高于已婚护理人员(18.27±12.21);各科室护理人员组织支持感总分与职业倦怠总分、抑郁倾向总分均呈负相关(均P＜0.05);职业倦怠总分与抑郁倾向总分呈正相关(r=0.325,P＜0.05).结论 职业倦怠在组织支持感和抑郁倾向之间起到中介作用,护理人员组织支持感对抑郁倾向起到直接预测作用.

目的 分析消化内科护士自我正念水平对工作厌倦和生活满足感的中介效应.方法 以北京某三级甲等医院在2019年6月消化内科工作的24名护士作为研究对象,使用一般数据资料调研表、自我正念觉察调研表、生活满意度调研表、护士工作厌倦调研表作为研究工具,对护士进行调查分析.结果 工作厌倦度对个体的生活满足感有反向预估作用(β=-0.268,P＜0.01);工作厌倦度对自我正念水平有明显的反向预估效应,方差净解释量为11.9％;回归分析结果表明,自我正念对生活满足感的影响明显(β=0.259,P＜0.01),方差净解释量为5.4％.自我正念水平在工作厌倦度与生活满足感的关联中起着部分中介调节作用,中介调节效应达-0.093,中介效应所占总效应比值为34.7％.结论 消化内科护士的自我正念能够缓冲工作厌倦,进而提高个体生活满足感,也是提升护士生活满足感的正导向因素.

Backgroud: Renal cell carcinoma (RCC) is one of the most common renal malignancies in the urinary system. Numerous studies have demonstrated that miRNAs can regulate tumorigenesis and progression, while the underlying molecular mechanism for miR-6838-5p involved in RCC development is still largely unknown.Methods: The relative expression of miR-6838-5p in RCC tissues, RCC cell lines, adjacent normal tissues and normal renal epithelial cells was detected by reverse transcription polymerase chain reaction (RT-qPCR). In vitro studies, cell proliferation and invasion in human RCC cell lines ACHN and 786-O were evaluated by CCK-8 assay, Transwell assay, Colony formation assay and Flow cytometry. Bioinformatics analysis, luciferase report analysis and Western blot assay were proved that Cyclin D binding myb-like transcription factor 1 (DMTF1) is the target of miR-6838-5p.Results: Our study confirmed that miR-6838-5p was upregulated in RCC tissues (30/42, 77.43%, P < 0.01) and RCC cell lines (P < 0.05) compared to adjacent normal tissues and normal renal epithelial cells. In vitro studies demonstrated that overexpression of miR-6838-5p significantly increased cell proliferation and invasion in human RCC cell lines ACHN and 786-O (P < 0.05), whereas inhibition of miR-6838-5p inhibited cell proliferation and invasion (P < 0.05). Furthermore, we found that miR-6838-5p binds to the wild-type DMTF1 3'UTR. In addition, we found that DMTF1 was downregulation in RCC tissues and cell lines. Meanwhile, it was demonstrated in ACHN cells that overexpression of miR-6838-5p inhibited the expression of DMTF1. Finally, we also confirmed that the interaction of miR-6838-5p overexpression and DMTF1 overexpression might rescue the inhibitory effects of overexpression of miR-6838-5p on the expression of phosphatase and tensin homolog (PTEN), p53, Murine double minute 2 (MDM2) and alternative reading frame (ARF) in the DMTF1-mediated ARF-p53 downstream pathway.Conclusions: Our research shows that miR-6838-5p enhances the growth and invasion of renal cell carcinoma dependent on DMTF1 via inhibiting the ARF-p53 pathway, which suggest that miR-6838-5p can be used as a marker for the diagnosis of RCC.

目的:观察二仙膏治疗精索静脉曲张性少精弱精症的疗效.方法:90例随机分为两组各45例,治疗组给予二仙膏治疗,对照组给予左卡尼汀治疗.结果:两组精子存活率、精子浓度、精子活力均提高(P＜0.05),治疗组各指标均优于对照组(P＜0.05).总有效率治疗组高于对照组(P＜0.05).结论:二仙膏治疗精索静脉曲张性少精弱精症疗效更好.

Objective:This research was aimed to explore protective effects of allicin on rat model of myocardial infarction via JNK signaling pathway.Methods:Rat myocardial ischemia model was established with subcutaneous injection of isoproterenol (ISO). Seventy-five rats were randomly divided into 5 groups (n= 15): sham group, ISO group, low-dose group (1.2 mg/kg/days for 7 days), medium-dose group (1.8 mg/kg/days for 7 days), and high-dose group (3.6 mg/kg/days for 7 days). Routine HE staining and Masson staining were performed to observe myocardial histopathology. The expression of oxidative stress-related indicators, heart tissue apoptosis-related proteins, and JNK and p-JNK proteins were measured for different groups.Results:Compared with the sham group, the T wave value of the ISO group was significantly increased (p <0.01). When allicin was administered, the T wave values at different time points in all groups were all decreased. Compared with the sham group, the ratio of eNOS, Bcl-2/Bax was significantly decreased, and p-eNOS, iNOS, caspase-3, caspase-9, and Cyt-c were significantly elevated in the ISO group (p <0.05). After allicin was administered, significant changes in these proteins were observed in the medium- and high-dose groups. There was no significant change in the expression of JNK protein in the ISO group compared with the sham group; however, the expression of eNOS and p-JNK protein were significantly upregulated (p <0.01) and the expression of p-eNOS and iNOS were significantly downregulated (p <0.01). When allicin was administered, expression of p-JNK protein was significantly downregulated.Conclusion:Allicin can reduce oxidative stress damage and cardiomyocyte apoptosis in rat model of myocardial infarction and can significantly regulate JNK signaling pathway.

Renal cell carcinoma (RCC) is the most common type of kidney cancer with rising incidence. Long noncoding RNA (lncRNA) LINC01133 is a novel lncRNA that is involved in the development of several types of cancers. However, the role of LINC01133 in RCC has not been reported. Thus, in this study, we investigated the functions of LINC01133 in RCC. The qualitative real-time polymerase chain reaction analysis was performed to examine the levels of LINC01133 in RCC tissues and adjacent tissues, as well as RCC cell lines. The results showed that LINC01133 was highly expressed in RCC tissue specimens and cell lines. Downregulation of LINC01133 significantly inhibited the proliferation, migration, and invasion of RCC cells. Further mechanistic investigations proved that LINC01133 directly interacted with microRNA (miR)-30b-5p and regulated the miR-30b-5p expression in RCC cell lines. Moreover, miR-30b-5p exhibited tumor-suppressive activity in RCC cell lines, which was mediated by targeting Ras-related protein Rab-3D (Rab3D). In vivo study showed that LINC01133 knockdown suppressed tumor growth in the nude mice. Taken together, these findings indicated that LINC01133 might be an oncogene in RCC through regulation of the miR-30b-5p/Rab3D axis. Thus, LINC01133 might serve as a potential therapeutic target for the treatment of RCC.