Lidocaine hampers colorectal cancer process via circITFG2/miR-1204/SOCS2 axis.

Colorectal cancer (CRC) is a deadly disease with a poor prognosis. Lidocaine is preferred by surgical procedures due to the excellent anesthesia. Circular RNA integrin alpha FG-GAP repeat containing 2 (circITFG2) has been recognized as a momentous participator in CRC progression. The specific role of circITFG2 was further studied in this research. Quantitative real-time PCR (qRT-PCR) was devoted to examining the expression of circITFG2, microRNA-1204 (miR-1204) and SOCS2 mRNA in CRC cells. Western blot was used to determine SOCS2 protein expression in CRC cells. Cell viability, colony formation and apoptosis were detected by cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry assay respectively. Cell migration and invasion were tested by wound healing assay and transwell assay. Dual-luciferase reporter system, RNA pull down and RNA-binding protein immunoprecipitation (RIP) assays were applied to verify the combination between miR-1204 and circITFG2 or SOCS2. CircITFG2 was strikingly downregulated; however, lidocaine treatment induced a significant increase in the expression of circITFG2 and SOCS2 and a decrease in miR-1204 expression in CRC cells. Meanwhile, SOCS2 protein expression was upregulated by lidocaine treatment or miR-1204 silence in CRC cells and downregulated by circITFG2 knockdown or miR-1204 overexpression in lidocaine-treated CRC cells. CircITFG2 knockdown or miR-1204 overexpression abolished lidocaine-induced inhibition in proliferation, metastasis and promotion in apoptosis in CRC cells. CircITFG2 overexpression, SOCS3 overexpression or lidocaine treatment suppressed proliferation, metastasis and facilitated apoptosis in CRC cells. CircITFG2 sponged miR-1204 to regulate SOCS3 expression in lidocaine-treated CRC cells. Lidocaine hindered CRC progression by circITFG2/miR-1204/SOCS2 axis. This finding might beat a path in improving CRC therapy.

Retracted: MicroRNA-495 Inhibits Gastric Cancer Cell Migration and Invasion Possibly via Targeting High Mobility Group AT-Hook 2 (HMGA2).

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study and the manuscript. Reference: Huashe Wang, Zhipeng Jiang, Honglei Chen, Xiaobin Wu, Jun Xiang, Junsheng Peng. MicroRNA-495 Inhibits Gastric Cancer Cell Migration and Invasion Possibly via Targeting High Mobility Group AT-Hook 2 (HMGA2). Med Sci Monit, 2017; 23: 640-648. DOI: 10.12659/MSM.898740.

EGF Relays Signals to COP1 and Facilitates FOXO4 Degradation to Promote Tumorigenesis.

Forkhead-Box Class O 4 (FOXO4) is involved in critical biological functions, but its response to EGF-PKB/Akt signal regulation is not well characterized. Here, it is reported that FOXO4 levels are downregulated in response to EGF treatment, with concurrent elevation of COP9 Signalosome subunit 6 (CSN6) and E3 ubiquitin ligase constitutive photomorphogenic 1 (COP1) levels. Mechanistic studies show that CSN6 binds and regulates FOXO4 stability through enhancing the E3 ligase activity of COP1, and that COP1 directly interacts with FOXO4 through a VP motif on FOXO4 and accelerates the ubiquitin-mediated degradation of FOXO4. Metabolomic studies demonstrate that CSN6 expression leads to serine and glycine production. It is shown that FOXO4 directly binds and suppresses the promoters of serine-glycine-one-carbon (SGOC) pathway genes, thereby diminishing SGOC metabolism. Evidence shows that CSN6 can regulate FOXO4-mediated SGOC gene expression. Thus, these data suggest a link of CSN6-FOXO4 axis and ser/gly metabolism. Further, it is shown that CSN6-COP1-FOXO4 axis is deregulated in cancer and that the protein expression levels of CSN6 and FOXO4 can serve as prognostic markers for cancers. The results illustrate a pathway regulation of FOXO4-mediated serine/glycine metabolism through the function of CSN6-COP1 axis. Insights into this pathway may be strategically designed for therapeutic intervention in cancers.

Ward nurses-focused educational intervention improves the quality of bowel preparation in inpatients undergoing colonoscopy: A CONSORT-compliant randomized controlled trial.

BACKGROUND: Adequate bowel preparation is essential for the detection of pathological lesions during colonoscopy. However, it has been found to be inadequate in approximately 20% to 30% of colonoscopy examinations. Educational interventions focused on health staff, such as physicians and nurses, may improve the patients' understanding of the bowel preparation instructions, and consequently, increase the quality of bowel preparation. OBJECTIVES: To investigate whether enhanced education of ward nurses could improve the bowel preparation quality in inpatients undergoing colonoscopy. DESIGN: This was a single-center randomized controlled study. METHODS: A total of 190 consecutive inpatients scheduled to undergo colonoscopy from March 2019 to March 2020 were randomized to the educated (nurses with enhanced education) or control group (nurses without enhanced education). We assessed the bowel preparation quality using the Boston bowel preparation scale. RESULTS: There were 89 patients in the educated group and 101 patients in the control group. The proportion of colonoscopies with adequate bowel preparation was 83.1% in the educated group and 69.3% in the control group. Patients' compliance with bowel preparation in the educated group was superior to that in the control group. Furthermore, significantly better sleep quality was found in the educated group. The multivariate logistic regression analysis identified the ward nurses-focused enhanced educational intervention as a risk factor for bowel preparation quality. CONCLUSIONS: The ward nurses-focused educational intervention improved the bowel preparation quality and reduced the adverse event rates in inpatients undergoing colonoscopy. TRIAL REGISTRATION: This study was registered in the Chinese Clinical Trial Registry under number ChiCTR2000030366.

Functional jejunal interposition versus Roux-en-Y anastomosis after total gastrectomy for gastric cancer: A prospective randomized clinical trial.

BACKGROUND: Nutritional status and quality of life deteriorate significantly after total gastrectomy for patients with gastric cancer. The numerous types of reconstruction proposed by medical researchers around the world have limited effect. This prospective, randomized clinical trial compared functional jejunal interposition with Roux-en-Y anastomosis to identify the optimal reconstruction procedure. METHODS: This was a multi-center, prospective, randomized control trial. The enrolled patients were randomly assigned into the functional jejunal interposition group and the Roux-en-Y group. All patients were followed up at regular intervals after surgery. The endpoints were postoperative nutritional status, quality of life, and long-term postoperative complications. RESULTS: A total of 113 patients were enrolled from August 2012 to September 2017. Until March 2018, the median follow-up period was 18 months. At 12 months after surgery, food intake per meal (P = 0.021), Prognosis Nutritional Index (P = 0.015), weight loss (P = 0.019), and Gastrointestinal Symptom Rating Scale score (P = 0.015) of the functional jejunal interposition group were significantly worse than those of the Roux-en-Y group. There was no significant difference in operative time, intraoperative blood loss, perioperative complications, time of first flatus and defecation after surgery, postoperative plasma nutritional parameters, Visick score, Eastern Cooperative Group physical condition score, and survival rate. CONCLUSION: For patients with long-term survival after total gastrectomy for gastric cancer, the Roux-en-Y anastomosis is a better choice compared with functional jejunal interposition.

Gastrointestinal endoscopy nurse assistance during colonoscopy and polyp detection: A PRISMA-compliant meta-analysis of randomized control trials.

BACKGROUND: Previous studies showed difference results about the effect of nurse in improvement of the colonoscopy detection rate. This meta-analysis aims to investigate whether nurse participation during colonoscopy can help in improving the detection rate of polyps and adenomas. METHODS: Original studies in English were searched from the MEDLINE database, PubMed, Web of Science, and the Cochrane Library database. Randomized control trials (RCT) comparing colonoscopy with and without nurse participation for the detection of colorectal polyps and adenomas were identified. A meta-analysis was performed using Revman 5.3 software. RESULTS: A total of 2268 patients from 4 RCTs were included in this meta-analysis. Outcomes of colonoscopy with nurse participation were compared with those of colonoscopy without nurse participation. The results showed that nurses' participation during colonoscopy could significantly increase both, polyp detection rate and adenoma detection rate. CONCLUSION: Nurse assistance during colonoscopy can help improve the rate of detection of polyps and adenomas.

Correction: CSN6-TRIM21 axis instigates cancer stemness during tumorigenesis.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Mining the role of RECQL5 in gastric cancer and seeking potential regulatory network by bioinformatics analysis.

AIM: The role of RecQ protein-like 5 (RECQL5) in gastric carcinoma (GC) is still unclear. Here, we investigated the role of RECQL5 in human GC and its potential regulatory network via bioinformatics analysis. METHODS: Bioinformatic analysis was performed using data in the Oncomine database, Kaplan- Meier Plotter online software, MethHC database, catalogue of somatic mutations in cancer (COSMIC), cbioportal database and String database. Then, we verified the association between RECQL5 expression and GC prognosis by immunohistochemistry (IHC). The independent prognostic factors were determined by Cox multivariate analysis. RESULTS: It was found that both the mRNA and protein expression levels of RECQL5 were downregulated in GC samples (P < .05). Low RECQL5 expression indicated a poor prognosis in GC patients and is the independent prognostic factors for GC. No correlation between RECQL5 mRNA and DNA methylation was found using the MethHC database. The analysis of the COSMIC database showed a high proportion of missense mutation in GC. The functional enrichment analysis predicted that RECQL5 plays a role in DNA repair and cellular responses to DNA damage stimulus. RECQL5 might be enriched in homologous recombination pathways and Fanconi anemia pathway. Bioinformatics analysis identified 5 genes, namely POLR2D, POLR2G, DXO, KIN, and EIF2D, that were significantly correlated with RECQL5. CONCLUSION: The low expression of RECQL5 predicts poor overall survival in GC. RECQL5 may be a novel tumor suppressor for patients with GC.

Nomogram for predicting pathological complete response to neoadjuvant chemotherapy in patients with advanced gastric cancer.

BACKGROUND: Survival benefit of neoadjuvant chemotherapy (NAC) for advanced gastric cancer (AGC) is a debatable issue. Studies have shown that the survival benefit of NAC is dependent on the pathological response to chemotherapy drugs. For those who achieve pathological complete response (pCR), NAC significantly prolonged prolapsed-free survival and overall survival. For those with poor response, NAC yielded no survival benefit, only toxicity and increased risk for tumor progression during chemotherapy, which may hinder surgical resection. Thus, predicting pCR to NAC is of great clinical significance and can help achieve individualized treatment in AGC patients. AIM: To establish a nomogram for predicting pCR to NAC for AGC patients. METHODS: Two-hundred and eight patients diagnosed with AGC who received NAC followed by resection surgery from March 2012 to July 2019 were enrolled in this study. Their clinical data were retrospectively analyzed by logistic regression analysis to determine the possible predictors for pCR. Based on these predictors, a nomogram model was developed and internally validated using the bootstrap method. RESULTS: pCR was confirmed in 27 patients (27/208, 13.0%). Multivariate logistic regression analysis showed that higher carcinoembryonic antigen level, lymphocyte ratio, lower monocyte count and tumor differentiation grade were associated with higher pCR. Concordance statistic of the established nomogram was 0.767. CONCLUSION: A nomogram predicting pCR to NAC was established. Since this nomogram exhibited satisfactory predictive power despite utilizing easily available pretreatment parameters, it can be inferred that this nomogram is practical for the development of personalized treatment strategy for AGC patients.

CSN6-TRIM21 axis instigates cancer stemness during tumorigenesis.

BACKGROUND: Cancer stem cells (CSCs) are responsible for tumour initiation, metastasis and recurrence. However, the mechanism of CSC formation, maintenance and expansion in colorectal cancer (CRC) remains poorly characterised. METHODS: The role of COP9 signalosome subunit 6 (CSN6) in regulating cancer stemness was evaluated by organoid formation and limited dilution analysis. The role of CSN6-TRIM21-OCT1-ALDH1A1 axis in CSC formation was evaluated in vitro and in vivo. The association of CSN6, TRIM21 and ALDH1A1 expression was validated by a tissue microarray with 267 CRC patients. RESULTS: The results showed that CSN6 is critical for sphere formation and maintaining the growth of patient-derived organoids (PDOs). We characterised the role of CSN6 in regulating cancer stemness, which involves the TRIM21 E3 ubiquitin ligase, transcription factor POU class 2 homeobox 1 (OCT1) and cancer stem cell marker aldehyde dehydrogenase 1 A1 (ALDH1A1). Our data showed that CSN6 facilitates ubiquitin-mediated degradation of TRIM21, which in turn decreases TRIM21-mediated OCT1 ubiquitination and subsequently stabilises OCT1. Consequently, OCT1 stabilisation leads to ALDH1A1expression and promotes cancer stemness. We further showed that the protein expression levels of CSN6, TRIM21 and ALDH1A1 can serve as prognostic markers for human CRC. CONCLUSIONS: In conclusion, we validate a pathway for cancer stemness regulation involving ALDH1A1 levels through the CSN6-TRIM21 axis, which may be utilised as CRC molecular markers and be targeted for therapeutic intervention in cancers.

Low expression of RecQ-like helicase 5 is associated with poor prognosis in patients with gastric cancer.

The role of RecQ-like helicase 5 (RECQL5) in gastric cancer (GC) is unclear. This study investigated the expression, clinicopathological association and prognosis of RECQL5 protein in human GC. Firstly, the Oncomine database was used to determine the mRNA expression levels of RECQL5 in GC samples. GC samples and adjacent normal gastric tissue samples were subsequently assessed to determine RECQL5 protein expression levels using immunohistochemistry. The clinicopathological association with RECQL5 expression was analyzed. Multivariate Cox analysis was performed to determine the relationship between RECQL5 expression and survival outcomes. Data from the Oncomine database revealed that RECQL5 mRNA was significantly downregulated in GC tissues compared with that in normal gastric tissues (P<0.05). These results were then validated at the protein level as RECQL5 protein expression was found to be significantly downregulated in GC samples compared with that in normal gastric tissues (P<0.05). Low expression of RECQL5 was significantly associated with depth of tumor invasion, histological differentiation and TNM stage (all P<0.05) and indicated poor prognosis in patients with GC. Multivariate analysis revealed that low RECQL5 expression and depth of invasion were independent prognostic factors for GC (P<0.05). These results suggest that low expression of RECQL5 is associated with carcinogenesis and invasion in GC and with poor overall survival in patients with GC. RECQL5 may be a novel prognostic marker for patients with GC.

LncRNA HAND2-AS1 inhibits 5-fluorouracil resistance by modulating miR-20a/PDCD4 axis in colorectal cancer.

BACKGROUND: Chemoresistance is one of the main obstacles in the therapy of human cancers, including colorectal cancer (CRC). Long non-coding RNA heart and neural crest derivatives expressed 2-antisense RNA 1 (lncRNA HAND2-AS1) has been demonstrated to be associated with CRC. However, the function of HAND2-AS1 in 5-Fluorouracil (5-FU) resistance of CRC remains unclear. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of HAND2-AS1, miR-20a and programmed cell death factor 4 (PDCD4) mRNA. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay was conducted to evaluate IC50 of 5-FU and cell proliferation. Flow cytometry analysis was used to determine cell apoptosis. Transwell assay was carried out to measure cell migration and invasion. Western blot assay was conducted to examine the protein levels of B-cell lymphoma-2 (Bcl-2), BCL2-Associated X (Bax), matrix metalloprotein 2 (MMP2), MMP9 and PDCD4. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull down assay were utilized to verify the combination between miR-20a and HAND2-AS1. Dual-luciferase reporter assay was used to analyze the association between miR-20a and PDCD4. Murine xenograft assay was used to confirm the function of HAND2-AS1 in vivo. RESULTS: HAND2-AS1 and PDCD4 were downregulated and miR-20a was upregulated in 5-FU-resistant CRC tissues and cells. HAND2-AS1 suppressed 5-FU resistance, cell proliferation, migration and invasion and promoted cell apoptosis in 5-FU-resistant CRC cells. HAND2-AS1 acted as a sponge of miR-20a to regulate PDCD4 expression. Moreover, HAND2-AS1 suppressed cell progression and 5-FU resistance by upregulating PDCD4 via sponging miR-20a in 5-FU-resistant CRC cells. Besides, HAND2-AS1 inhibited tumor growth in vivo. CONCLUSION: HAND2-AS1/miR-20a/PDCD4 axis inhibited cell progression and 5-FU resistance in 5-FU-resistant CRC cells.

Analysis of TGCA data reveals genetic and epigenetic changes and biological function of MUC family genes in colorectal cancer.

Aim: Few studies focused on functions and regulatory networks of MUC family members in colorectal cancer based on comprehensive analysis of online database. Materials & methods: Copy number variation, methylation, pathway analysis and drug influence on MUC expression were analyzed based on The Cancer Genome Atlas and GTEx database. Results: Copy number variation analysis showed MUC heterozygous amplification and heterozygous deletion predominate. Methylation of MUC17, MUC12 and MUC4 were found related to gene expression. Function of MUC family genes mainly affects pathways such as apoptosis, cell cycle, DNA damage and EMT pathways. PLX4720, dabrafenib, gefitinib, afatinib and austocystin D can alter the expression of MUC gene. Conclusion: The genetic and epigenetic changes of MUC are related to the level of MUC expression in colorectal cancer.

ROS-mediated inactivation of the PI3K/AKT pathway is involved in the antigastric cancer effects of thioredoxin reductase-1 inhibitor chaetocin.

Novel drugs are urgently needed for gastric cancer (GC) treatment. The thioredoxin-thioredoxin reductase (TRX-TRXR) system has been found to play a critical role in GC tumorigenesis and progression. Thus, agents that target the TRX-TRXR system may be highly efficacious as GC treatments. In this study, we showed that chaetocin, a natural product isolated from the Chaetomium species of fungi, inhibited proliferation, induced G2/M phase arrest and caspase-dependent apoptosis in both in vitro and in vivo models (cell xenografts and patient-derived xenografts) of GC. Chaetocin inactivated TRXR-1, resulting in the accumulation of reactive oxygen species (ROS) in GC cells; overexpression of TRX-1 as well as cotreatment of GC cells with the ROS scavenger N-acetyl-L-cysteine attenuated chaetocin-induced apoptosis; chaetocin-induced apoptosis was significantly increased when GC cells were cotreated with auranofin. Moreover, chaetocin was shown to inactivate the PI3K/AKT pathway by inducing ROS generation; AKT-1 overexpression also attenuated chaetocin-induced apoptosis. Taken together, these results reveal that chaetocin induces the excessive accumulation of ROS via inhibition of TRXR-1. This is followed by PI3K/AKT pathway inactivation, which ultimately inhibits proliferation and induces caspase-dependent apoptosis in GC cells. Chaetocin therefore may be a potential agent for GC treatment.

Integrin subunit alpha V promotes growth, migration, and invasion of gastric cancer cells.

Integrin subunit alpha V (ITGAV), a member of integrin family of extracellular matrix receptors, is involved in many types of cancer. In this study, the expression levels, clinical features and prognosis of ITGAV in gastric cancer (GC) patients were investigated, and the functional roles of ITGAV were also investigated. Cell Counting Kit-8 (CCK-8) assay was performed to examine the proliferation of GC cells. Transwell assays and wound-healing assays were conducted to explore the effect of ITGAV expression on GC cell migration and invasion. We found that ITGAV was overexpressed in both GC tissues and GC cells. ITGAV expression was positively correlated with lymph node metastasis and TNM stage of GC. High expression of ITGAV was associated with shorter overall survival (OS) and disease-free survival (DFS). Interestingly, the downregulation of ITGAV resulted in suppression of proliferation, migration, and invasion in GC cells. In conclusion, ITGAV is overexpressed in gastric cancer and is associated with poorer prognostic outcomes. ITGAV may serve as an important prognostic marker for GC staging and progression.

Predictability of gastric intestinal metaplasia by patchy lavender color seen on linked color imaging endoscopy.

We aimed to investigate the ability of linked color imaging (LCI) versus white light endoscopy (WLE) to detect gastric intestinal metaplasia (GIM). One hundred and seven participants who underwent upper gastrointestinal endoscopy were included. Under WLE endoscopy, biopsies were performed on any suspected abnormal mucosal changes. Under LCI endoscopy, we tested whether the specific color feature of patchy lavender color (PLC) pathologically indicated GIM. Biopsies were randomly performed in participants who had neither PLC nor suspected lesions. The detection abilities of LCI and WLE were assessed by comparison of histological and endoscopic findings. A total of 41 participants had histological GIM. The total diagnostic accuracy rate for GIM by LCI was 79.44%, higher than that of WLE (40.19%) (P < 0.001). Moreover, LCI with targeted biopsies showed a significantly increased ability to detect GIM (P < 0.001). PLC observed in the gastric mucosa on LCI can guide endoscopic biopsies and increase the detection rate of GIM. Thus, LCI could be a good tool for detecting GIM. ClinicalTrials.gov Identifier: ChiCTR-DDD-17011326).

Toosendanin induces caspase-dependent apoptosis through the p38 MAPK pathway in human gastric cancer cells.

Although many advances have been made in the treatment of gastric cancer (GC), numerous difficulties, such as the emergence of chemo-drug resistance, continue to lead to disappointing GC prognoses. Thus, novel alternative strategies are urgently needed. The use of natural products could be a viable option to treat GC. Toosendanin (TSN) is a triterpenoid derived from the bark of Melia toosendanin Sieb. et Zucc that has been shown to be highly cytotoxic to multiple cancer cells. As the underlying impact of TSN on GC and its molecular mechanism remain poorly understood, in this study, we performed a series of experiments involving the use of TSN to treat GC cells. In the present study, we showed that TSN suppressed cell viability, inhibited cell proliferation by causing G1/S arrest and induced caspase-dependent apoptosis in AGS and HGC-27 cells. The possible mechanism of TSN-induced apoptosis may be associated with the activation of the p38 MAPK pathway. These results demonstrated the potential of TSN as a promising therapeutic compound to treat gastric cancer.

Overexpression of RECQL4 is associated with poor prognosis in patients with gastric cancer.

The present study aimed to investigate the expression, clinical association, and prognosis of RecQ protein-like 4 (RECQL4) protein in human gastric cancers (GCs). The expression levels and prognostic value of RECQL4 were initially predicted by using bioinformatics. GC specimens and matched normal gastric tissues were evaluated by immunohistochemistry (IHC), and patient clinicopathological parameters and survival times were analyzed. Multivariate Cox analysis was used to determine the prognostic role of RECQL4 expression. The Oncomine database predicted that RECQL4 mRNA expression levels were significantly increased in GCs as compared with those in normal gastric tissues (P<0.05) and that patients with increased RECQL4 mRNA expression levels had significantly lower overall survival (OS) (P<0.001). The results of IHC showed that the positive rate of RECQL4 in the GC samples was significantly higher than that in the normal gastric mucosa specimens (P<0.05). RECQL4 expression was positively associated with depth of invasion and TNM (P<0.05). High RECQL4 expression in GC samples was significantly associated with poor OS (P=0.024). Positive RECQL4 expression, depth of invasion, lymphatic invasion, and TNM staging were independent factors for predicting worse OS rates by using multivariate analysis. Compared with expression levels in normal gastric tissues, RECQL4 was significantly overexpressed in GC samples, and increased RECQL4 expression was an independent predictor of poor prognosis in GC patients.

[Complications analysis of subcutaneous venous access port for chemotherapy in patients with gastrointestinal malignancy].

OBJECTIVE: To describe and analyze the complications of subcutaneous venous access port for patients with gastrointestinal malignancy. METHODS: Data of 1 912 patients with gastrointestinal malignancy who accepted chemotherapy in our department via subcutaneous venous access ports, including 127 cases in upper arm, 865 cases in subclavicular vein and 920 cases in internal jugular vein, from June 2007 to April 2016 were analyzed retrospectively. Associated complications and risk factors were emphatically investigated. RESULTS: Postoperative complications were confirmed in 233 patients(12.2%), and complication morbidity was 37.0%(47/127), 15.5%(134/865), 6.7%(62/920) in upper arm group, subclavicular vein group, internal jugular vein group respectively, whose difference was statistically significant (χ2=71.060, P=0.000). Sixty-one(3.2%) patients developed early complications (in the day of insertion, including catheter dislocation, pneumothorax, arterial damage). Early complication morbidity of upper arm group (14.2%, 18/127) was higher as compared to subclavicular vein group (3.4%, 29/865) and internal jugular vein group(1.5%, 14/920) with significant difference (χ2=57.867, P=0.000). Postoperative long-term complications (catheter dislocation, thrombosis, pinch-off syndrome, infusion base exposure, catheter detachment) were found in 182(9.5%) patients. Morbidity of long-term complication was 5.2%(48/920) in internal jugular vein group, which was significantly lower than 22.8% (29/127) in upper arm group and 12.1% (105/865) in subclavicular vein group with statistically significant difference (χ2=50.828, P=0.000). Multivariate analysis indicated that subclavicular vein intubation (OR=0.536, 95%CI: 0.341 to 0.843; P=0.007 OR=0.156, 95%CI: 0.096 to 0.253, P=0.000), internal jugular vein intubation (OR=0.156, 95%CI: 0.096 to 0.253, P=0.000), operation time <40 minutes (OR=0.458, 95%CI: 0.342 to 0.613, P=0.000) and standardized training (OR=0.233,95%CI: 0.171 to 0.318, P=0.000) were protective factors of postoperative complication; besides, subclavicular vein intubation (OR=0.458, 95%CI: 0.342 to 0.613, P=0.000), internal jugular vein intubation (OR=0.233, 95%CI: 0.171 to 0.318, P=0.000) and standardized training (OR=0.313, 95%CI: 0.173 to 0.568, P=0.000) were protective factors of thrombosis. CONCLUSIONS: Subcutaneous venous access port implantation is a preferable access to central vein. Appropriate intubation approach and standardized training may reduce postoperative complications effectively. Internal jugular vein approach is safer and more reliable than upper arm vein and subclavian vein approach.