Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 3C, the immunohistochemical data shown in Fig. 4B and the western blots in Fig. 5B had already been submitted to, or were published in, articles in other journals that featured some of the same authors; moreover, some of these data subsequently appeared in different articles in other journals that were not connected with either this research group or this research topic. Upon investigating these issues further in the Editorial Office, it was noted that, concerning Figs. 3‑5 and as far as those papers sharing some of the same authors was concerned, the cases of data sharing weren't necessarily as simple as the data merely being duplicated. Given the sharing of these contentious data across a number of different journals, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 32: 1571‑1577, 2024; DOI: 10.3892/or.2014.3386].

Recent studies have reported that microRNA-526b (miR-526b) is implicated in the growth and metastasis of cancer cells. However, the clinical significance of miR-526b and its role as well as underlying mechanisms are largely unknown in hepatocellular carcinoma (HCC). Here, we detected miR-526b expression difference between HCC and matched nontumor tissues with qRT-PCR. We found that miR-526b displayed lower expression in HCC patient tissues and cells. Clinical analysis revealed that low miR-526b expression correlated with large tumor size, venous infiltration, advanced tumor-node-metastasis (TNM) stage. Furthermore, miR-526b underexpression independently predicted poor prognosis of HCC patients. Functionally, we demonstrated that miR-526b inhibited proliferation, migration and invasion of HCC cells in vitro. Moreover, miR-526b overexpression restrained the tumor growth and pulmonary metastasis in vivo. Mechanistically, we proved that miR-526b could directly bind to 3'UTR of sirtuin 7 (SIRT7) mRNA and repressed its expression. miR-526b and SIRT7 showed a negative correlation in HCC tissues. More importantly, up-regulating SIRT7 expression antagonized miR-526b-inhibited proliferation, migration and invasion in SMMC-7721 cells. Furthermore, miR-526b suppressed epithelial-to-mesenchymal transition (EMT) of HCC cells. Immunoblotting analysis indicated that miR-526b reduced the levels of phosphorylated ERK (p-ERK), c-Myc, Cyclin D1, c-Jun, SNAIL and SLUG in HCC cells. SIRT7 restoration promoted phosphorylation of ERK and EMT in miR-526b overexpressing SMMC-7721 cells. Taken together, this is the first time we demonstrated that miR-526b might function as a prognostic biomarker and suppressed SIRT7 expression, and subsequently led to the growth and metastasis of HCC. Our findings provide miR-526b/SIRT7 axis as a promising drug target for HCC.

BACKGROUND:Fibulin-5 has been considered as a tumor suppressor through inhibiting tumor growth and invasion. Reduced expression of Fibulin-5 is frequently observed in various human cancers. In this study, we investigate the clinical significance of Fibulin-5 and its role in hepatocellular carcinoma (HCC) cell migration and invasion. METHODS:The expression of Fibulin-5 was evaluated by qRT-PCR and immunoblotting in HCC and matched noncancerous tissues. Fibulin-5 was over-expressed or knocked down by a retrovirus-mediated expression plasmid or a specific siRNA in HCC cells. Boyden chamber and Transwell assays were used to test HCC cell migration and invasion. Immunostaining was performed to determine matrix metalloproteinase-7 (MMP-7) expression in HCC specimens. MMP-7 retroviruses and siRNA were used to alter MMP-7 expression in HCC cells. RESULTS:In our study, the expression levels of Fibulin-5 protein and mRNA were down-regulated in HCC tissues as compared with those in matched noncancerous tissues. Reduced expression of Fibulin-5 was observed in all HCC cell lines (HepG2, SMMC-7721, MHCC97L, Hep3B, MHCC97H and HCC-LM3) as compare with that in a non-transformed hepatic cell line (LO2). Low expression of Fibulin-5 was significantly correlated with poor prognostic features including multiple tumor nodes, venous infiltration, high Edmondson-Steiner grading and advanced tumor-node-metastasis (TNM) tumor stage. Furthermore, we demonstrated that Fibulin-5 was a novel independent prognostic marker for predicting 5-year survival of HCC patients. Our in vitro studies showed that Fibulin-5 overexpression inhibited HCC cell migration and invasion. While Fibulin-5 knockdown increased the number of migrated and invaded HCC cells. Fibulin-5 negatively regulated MMP-7 abundance in HCC cells. Moreover, the inverse correlation between Fibulin-5 and MMP-7 expressions was observed in HCC tissues. Mechanistically, we disclosed that MMP-7 knockdown reduced the number of migrated and invaded HCC cells. Restoring MMP-7 expression abrogated the suppressive effect of Fibulin-5 on HCC cell migration and invasion in vitro, suggesting that Fibulin-5 exerted its anti-metastatic function, at least in part, by down-regulating the expression of MMP-7 in HCC cells. CONCLUSIONS:These results indicate that Fibulin-5 may serve as a prognostic biomarker and inhibits HCC invasion and metastasis by suppressing MMP-7 expression.

目的 探讨微信小程序在术前达芬奇机器人管理中的应用效果.方法 选取2019年1-12月医院的610台达芬奇机器人手术,按照术前器械管理方法不同分组,2019年1-6 月的 293 台达芬奇机器人手术采用传统方法进行开台准备为对照组,2019 年 7-12 月的317台达芬奇机器人手术采用微信小程序进行开台准备为观察组.比较两组术前器械准备差错发生率、术前准备耗费的时间、器械清洗成本、器械纸塑高温包装及灭菌处理成本.结果 观察组术前器械准备差错率、术前准备浪费的时间及器械清洗、器械纸塑高温包装和灭菌处理成本低于对照组,差异有统计学意义(P<0.05).结论 在术前达芬奇机器人的器械管理中应用微信小程序能有效降低器械准备差错发生率,缩短术前准备时间,并降低器械使用成本.

目的 探讨利伐沙班预防脾切除术后门静脉血栓(PVT)形成的作用机制.方法 将82例接受脾切除术的患者随机分为利伐沙班组(n=41)和对照组(n=41).利伐沙班组给予利伐沙班,对照组给予低分子肝素联合华法林.两组患者术后均随访6个月.比较两组的术后PVT发生情况、凝血相关指标、用药安全性及患者耐受性、生存率.结果 术后6个月,利伐沙班组的PVT发生率明显低于对照组,差异具有统计学意义(P<0.05).利伐沙班组的PVT发生率为43.9％,明显低于对照组的80.5％,差异具有统计学意义(P<0.05).术后1周及1个月,利伐沙班组的凝血酶原时间(PT)长于对照组,蛋白C(PC)和蛋白S(PS)水平均明显高于对照组,差异具有统计学意义(P<0.05).两组术后6个月内肝功能失代偿及肝癌发生率均无显著差异(P>0.05).两组患者均对药物耐受,随访6个月内未出现死亡病例.结论 预防性使用利伐沙班可显著降低脾切除术后PVT发生率.对患者PC和PS的保护作用可能是利伐沙班预防PVT发生的重要作用机制之一.

Background: Hypoxia critically drives malignant tumor development and is characteristic of hepatocellular carcinoma (HCC), where HIF-1 alpha plays a crucial role. The ubiquitin-conjugating enzyme E2K (UBE2K) is known to participate in the advancement of several human cancers. However, the role of UBE2K in HCC or whether it is a hypoxia-responsive gene remains to be further identified. Method: We performed a microarray to measure the gene expression differences between normoxia and hypoxia. CoCl2 mimicked the hypoxic condition. The protein and RNA expression of HIF-1 alpha, UBE2K, and Actin in HCC cells were measured by western blotting(WB) and RT-qPCR, respectively. Immunohistochemical (IHC) staining analyzed the expression of UBE2K and HIF-1 alpha in HCC tissues. CCK-8 and colony formation assay evaluated the HCC cell growth. Scratch healing and transwell assays were used to detect the migration capability of the cells. Lipofectamine 3000 was used to transfect the plasmids or siRNAs to HCC cells. Results: We identified UBE2K as a potential hypoxia-responsive gene. Our study showed that hypoxia induced HIF-1 alpha-mediated increase of UBE2K levels in HCC cells, which decreased under HIF-1 alpha deficiency under hypoxia. Further bioinformatics analysis based on UALCAN and GEPIA databases confirmed that UBE2K was highly expressed in HCC tissues and positively associated with HIF-1 alpha expression. Functionally, Hep3B and Huh7 cell proliferation and migration were stimulated upon UBE2K overexpression, while the UBE2K knockdown suppressed such effect. Furthermore, functional rescue experiment proved that depletion of UBE2K inhibited hypoxia-induced cell proliferation and migration in HCC cells. In contrast, enhancing UBE2K levels rescued cell proliferation and migration repression caused by HIF-1 alpha deficiency in hypoxia. Conclusion: Our results established UBE2K as a potential hypoxia-inducible gene in HCC cells, positively regulated by HIF-1 alpha in hypoxia. Moreover, UBE2K served as an oncogene and cooperated with HIF-1 alpha to form a functional HIF-1 alpha/UBE2K axis to trigger HCC progression, highlighting a potential application of UBE2K as a therapeutic target for HCC treatment.

Hepatocellular carcinoma (HCC) is a serious threat to human health and life due to its high morbidity and mortality. Ubiquitin-conjugating enzymes are players in the ubiquitin proteasome system and are responsible for a great number of physiological activities in cells. The action of ubiquitin-conjugating enzyme UBE2K in HCC has not been reported. Therefore, we studied the function and role of UBE2K in the malignant progression of HCC. An analysis of UBE2K expression in HCC cells was performed using RT-qPCR and protein immunoblotting. CCK-8, Transwell and sphere formation assays were used to identify the potential effects of UBE2K in HCC cell proliferation, migration and stemness property. RT-qPCR, and protein immunoblotting experiments was taken to explore the regulation between UBE2K and c-Myc. Here, we discovered that UBE2K expression was elevated in HCC cells, and elevated UBE2K predicts worse prognosis for HCC patients. Functionally, UBE2K promote, while UBE2K knockdown suppressed cell proliferation, migration and stemness property of HCC cells. Furthermore, c-Myc was identified as a downstream target of UBE2K. Moreover, functional rescue experiments finally proved that UBE2K facilitates the malignant progression of HCC cells by upregulating c-Myc. We clarified through in vivo experiments that UBE2K expression promotes tumor growth in HCC. Taken together, our study results proved the molecular regulation of UBE2K and c-Myc in HCC and the oncogenic role of UBE2K/c-Myc axis in HCC progression, thus it provides a promising molecular target for the diagnosis and treatment of HCC.

Conversion therapy has become the core in the treatment of borderline resectable or unresectable liver cancer, which provides resectable opportunities for more advanced liver cancer patients. In accordance with the first-choice treatment regimen recommended by the guidelines, the authors reported a successful case of Atezolizumab and Bevacizumab (T+A regimen) conversion therapy. The patient with initially borderline resectable advanced liver cancer was performed liver segment resection sucessfully after conversion therapy, and non-tumor recurrence was observed at postoperative 9 months. Postoperative pathological examination showed combined hepatocellular-cholangiocarcinoma, which also indicated the important value of T+A regimen in the conversion therapy of combined hepatocellular-cholangiocarcinoma.

Objective:To analyze the clinical features and prognosis of liver perivascular epithelioid cell neoplasms (PEComa).Methods:The clinical data of 12 patients with liver PEComa diagnosed by pathology at the First Affiliated Hospital of Xi 'an Jiaotong University from October 2011 to November 2021 were retrospectively analyzed. There were 1 male and 11 females, with a median age of 44 (range 20 to 63) years old. The clinical manifestations, laboratory examinations, imaging features, treatment methods, postoperative pathological features and treatment outcomes of these patients were collected and analysed. Postoperative follow-up by telephone or patient's follow-up records.Results:Among the 12 patients with hepatic PEComa, 8 patients (66.7%) were asymptomatic and 11 patients (91.7%) had a single lesion. All patients underwent surgical treatment, including local tumor resection in 10 patients (83.3%) and extended hemihepatectomy in 2 patients (16.7%). Enhanced CT showed the lesion to be a quasi-round homogeneous low-density mass, enhanced in arterial phase with hepatic artery branches in the lesion, and decrease in enhancement degrees in portal vein phase and delayed phase. Postoperative pathology of the lesions in all the 12 patients was benign. Immunohistochemical results showed that the positive rates of melanoma cell markers HMB45, Melan-A and smooth muscle actin were 100.0%(12/12), 83.3%(10/12) and 91.7%(11/12) respectively. The median follow-up period was 27 months, and no recurrence or metastasis was found.Conclusion:Hepatic PEComa occurred commonly in women with obscure symptoms. The lesion was mainly single and it had no correlation with hepatitis. It is easily confused with primary liver cancer and liver metastasis on medical imagings. PEComa expressed markers of both melanocyte and smooth muscle cell, and radical surgical resection resulted in good results.

The hypoxic tumor microenvironment, a fundamental feature of solid tumors, drives hepatocellular carcinoma (HCC) progression through regulating the transcriptional activities of protein-coding and noncoding genes. However, long noncoding RNA (lncRNA)-mediated HCC progression in hypoxic microenvironment remains largely unknown yet. In this study, we found that LINC00674 was upregulated under hypoxic conditions in a HIF-1-dependent manner, and the occupancy of HIF-1 to HRE of LINC00674 gene promoter was essential for its transcription. In addition, LINC00674 level was increased in HCC cell lines and tissues. Clinically, statistical analysis showed that LINC00674 expression was significantly associated with tumor size, venous infiltration, tumor stage and poor prognosis of HCC. Functionally, loss-of-function assays revealed that LINC00674 knockdown inhibited the migration, proliferation and invasion of HCC cells. Furthermore, LINC00674 silencing prominently repressed the mTOR signaling pathway. LINC00674 overexpression-enhanced HCC cell proliferation, migration and invasion were markedly abolished by an mTOR inhibitor rapamycin. NADPH oxidase 1 (NOX1) was positively regulated by LINC00674 in HCC cells. NOX1 knockdown markedly reversed LINC00674-upregulated the p-mTOR level and HCC cells' malignant behaviors. Finally, we found that LINC00674 knockdown attenuated the growth of HCC cells in vivo. Our finding demonstrated that LINC00674 was a new HIF-1 target gene, and hypoxia-induced LINC00674 exerted a pro-proliferative and pro-metastatic role in HCC, possibly by activating the NOX1/mTOR signaling pathway. This study suggested LINC00674 as a promising therapeutic target for HCC.

腹腔镜胆囊切除术(laparoscopic cholecystec-tomy,LC)作为胆囊结石或合并胆囊炎治疗的金标准已经毋庸置疑,也是普外科最为常见及最为容易学习的手术之一.临床调查显示,近年我国胆囊疾病发病率逐年上升[1],但是由于解剖变异等各种原因造成LC术中医源性胆管损伤(IBI)却是屡见不鲜,经多个系统回顾分析,目前腹腔镜下胆囊切除术后胆道损伤发生率为0.32％～0.52％[2].而胆囊三角区(Colot三角)解剖不清是导致手术并发症尤其是胆道损伤的主要原因之一[3].作者在临床实践中采用优先解剖分离胆囊管的LC术治疗胆囊结石或合并胆囊炎,取得了较好的手术效果,现报告如下.

Long non-coding RNAs (lncRNAs) are critical drivers and suppressors of human hepatocellular carcinoma (HCC). The downregulation of transmembrane protein 220 antisense RNA 1 (TMEM220-AS1) is correlated with poor prognosis in HCC. Nevertheless, the role of TMEM220-AS1 in HCC and the underlying mechanism remains unclear. In this study, TMEM220-AS1 levels were markedly reduced in HCC tissues compared with noncancerous tissues. TMEM220-AS1 downregulation was confirmed in HCC cell lines. TMEM220-AS1 expression was associated with tumor stage, venous infiltration, tumor size, and survival of HCC patients. TMEM220-AS1 overexpression suppressed the migration, invasion, and proliferation of HCC cells. Interestingly, ectopic expression of TMEM220-AS1 increased TMEM220 levels in HCC cells. Decreased TMEM220 levels were observed in HCC tissues and cell lines. TMEM220 expression was positively correlated with TMEM220-AS1 levels in HCC tissue samples and TMEM220 downregulation was significantly correlated with reduced patient survival. TMEM220 overexpression suppressed HCC cell proliferation and mobility. TMEM220 knockdown eliminated the suppressive effect of TMEM220-AS1 in HCCLM3 cells. Mechanistically, TMEM220 overexpression reduced the nuclear accumulation of β-catenin and decreased MYC, Cyclin D1, and Snail1 mRNA levels in HCCLM3 cells. BIO, a GSK3β inhibitor, eliminated TMEM220-induced Wnt/β-catenin pathway inactivation and inhibited HCC cell proliferation and mobility. In conclusion, TMEM220-AS1 and TMEM220 were expressed at low levels in HCC patients. TMEM220-AS1 inhibited the malignant behavior of HCC cells by enhancing TMEM220 expression and subsequently inactivating the Wnt/β-catenin pathway.

The ubiquitin-conjugating enzyme (E2) is a critical component of the ubiquitin-proteasome system and regulates hepatocarcinogenesis by controlling protein degradation. Ubiquitin-conjugating enzyme E2 O (UBE2O), a member of the E2 family, functions as an oncogene in human cancers. Nevertheless, the role of UBE2O in hepatocellular carcinoma (HCC) remains unknown yet. Here, we demonstrated that the UBE2O level was markedly upregulated in HCC compared with adjacent noncancerous tissues. UBE2O overexpression was also confirmed in HCC cell lines. UBE2O overexpression was prominently associated with advanced tumor stage, high tumor grade, venous infiltration, and reduced HCC patients' survivals. UBE2O knockdown inhibited the migration, invasion, and proliferation of HCCLM3 cells. UBE2O overexpression enhanced the proliferation and mobility of Huh7 cells. Mechanistically, UBE2O mediated the ubiquitination and degradation of AMP-activated protein kinase α2 (AMPKα2) in HCC cells. UBE2O silencing prominently increased AMPKα2 level and reduced phosphorylated mechanistic target of rapamycin kinase (p-mTOR), MYC, Cyclin D1, HIF1α, and SREBP1 levels in HCCLM3 cells. UBE2O depletion markedly activated the AMPKα2/mTOR pathway in Huh7 cells. Moreover, AMPKα2 silencing reversed UBE2O downregulation-induced mTOR pathway inactivation. Rapamycin, an inhibitor of mTOR, remarkably abolished UBE2O-induced mTOR phosphorylation and HCC cell proliferation and mobility. To conclude, UBE2O was highly expressed in HCC and its overexpression conferred to the poor clinical outcomes of patients. UBE2O contributed to the malignant behaviors of HCC cells, including cell proliferation, migration, and invasion, by reducing AMPKα2 stability and activating the mTOR pathway.

目的:探讨腹腔镜下经胆囊管途径治疗胆总管结石的可行性、安全性.方法:回顾分析2015年1月至2018年1月为135例胆囊结石合并胆总管结石患者行腹腔镜手术的临床资料,其中65例行腹腔镜经胆囊管胆总管探查取石术(LTCBDE);70例行腹腔镜胆总管探查取石术(LCBDE).对比两组患者一般情况、手术时间、术中出血量、腹腔引流时间、住院时间、住院费用、并发症发生率.结果:两组患者一般情况、术后并发症发生率差异无统计学意义(P>0.05),LTCBDE组术后住院时间、术后腹腔引流时间、住院费用、手术时间优于LCBDE组(P<0.05).结论:LTCBDE可避免术后T管引流,提高生活质量,缩短住院时间,具有经济优势.

This study aimed to evaluate the safety and efficacy of rivaroxaban in preventing portal vein system thrombosis (PVST) in patients with liver cirrhosis after splenectomy and pericardial devascularization. 70 cirrhotic patients undergoing splenectomy and pericardial devascularization were randomly assigned to rivaroxaban treatment (n=35) or low-molecular weight heparin (LMWH) plus warfarin treatment (n=35) for 30 days in this randomized controlled trial. The primary endpoint is the PVST formation. Ultrasound doctors and radiologists were blinded to the randomization results. Both groups received routine outpatient inspection every month and were followed for one year. 17 patients (48.6 %) in rivaroxaban group developed PVST, compared with 27 patients (77.1 %) in LMWH plus warfarin group (P=0.025). The incidence of PVST during the first year postoperation was significantly lower in rivaroxaban group than in LMWH plus warfarin group (F=7.901, P=0.006). The intra-group comparisons versus baseline showed the liver function improved from POD 21 to POM 1, and coagulation function improved from POM 2, in rivaroxaban group. In contrast, the liver function improved from POM 1 to POM 2, and coagulation function improved from POM 4, in LMWH plus warfarin group. The prophylactic use of rivaroxaban significantly decreases the incidence of PVST after splenectomy and pericardial devascularization in cirrhotic patients compared to LMWH plus warfarin treatment. Besides, rivaroxaban treatment was safe and effective and associated with better liver and coagulation functions improvement than LMWH plus warfarin treatment.

目的 探讨三维可视化及虚拟手术技术在住院医师肝脏手术规范化培训教学中的作用及效果.方法 选取西安交通大学第一附属医院肝胆外科的40名住院医师(包括规范化培训住院医师、进修医师及该院医师)作为研究对象,随机分为对照组(n=20)和试验组(n=20).对照组采用传统的肝脏解剖、手术图谱及二维的CT或MRI图像进行手术规划及手术路径制定的教学;试验组采用重建软件生成的肝脏三维重建可视化模型及虚拟手术模块,结合高清手术录像进行教学.教学结束后对两组住院医师进行考核评分,评价其手术规划能力及对手术路径的理解力,最后进行问卷调查,评价住院医师对教学方法的体会及满意度.结果 试验组手术规划及手术路径理解的考核总得分为(7.450±1.468)分,显著优于对照组的(4.950±1.146)分,差异具有统计学意义(P＜0.01);试验组对肝脏病变与肝动脉、门静脉、肝静脉、胆道关系的判断正确率显著高于对照组,试验组制定的切肝平面准确率显著高于对照组(P＜0.01).试验组对肝脏外科手术教学的兴趣及满意度显著高于对照组(P＜0.05).结论 采用三维可视、虚拟手术技术进行住院医师肝脏外科手术教学,可显著提升住院医师对复杂肝脏手术的术前规划能力和对手术路径的理解能力,值得推广.

Objective:To summarize the experience of laparoscopic concurrent surgery in the treatment of colon cancer liver metastasis and pelvic metastasis, and to explore its safety and feasibility in the treatment process.Methods:A retrospective analysis of the clinical data and diagnosis and treatment process of a patient with liver metastasis from colon cancer and pelvic metastasis in the First Affiliated Hospital of Xi′an Jiaotong University in Jun. 2021.Results:The patient received simultaneous laparoscopic resection of the right colon for liver metastatic cancer, complete hysterectomy and bilateral adnexectomy, and R0 resection was successfully achieved. The total operative time was 330 min, and the bleeding was 100 ml. Peritoneal hyperthermic perfusion chemotherapy was assisted. Pathological results showed that colonic ulcerative moderately differentiated adenocarcinoma invaded the deep myometrium of the uterine wall and bilateral ovarian cervix, infiltrated in liver tissue, and metastatic in periintestinal lymph nodes (2/30). The abdominal CT and tumor markers showed no abnormalities one month after the operation. At present, the patient is continuing to follow up closely.Conclusions:Simultaneous laparoscopic surgery is safe and feasible for the treatment of colon cancer liver metastases and pelvic metastases. It also has the advantages of less trauma, fast recovery, and beautiful incisions. The MDT mode plays an important role in improving the clinical benefits of patients and is worthy of promotion.