Background Dysphagia is a major symptom in esophageal carcinoma (EC) patients. photodynamic therapy (PDT) was approved for palliative treatment of patients with obstructive EC. Although it can remove the obstruction quickly, PDT may be difficult to achieve eradication alone. Thus, we aimed to assess whether photodynamic therapy sequential Dose-Reduction concurrent chemoradiotherapy (CCRT) can be an effective and safe approach for locally advanced obstructive EC. Methods This retrospective study included 121 patients with locally advanced obstructive EC who treated with radical CCRT (conventional treatment) and PDT sequential dose-reduction CCRT (combined treatment). A 1:1 propensity score matching (PSM) was conducted to balance potential bias. The improvement of dysphagia and overall survival (OS) was analyzed as the primary endpoint. Progression-free survival (PFS), local control, nutritional improvement and toxicities were analyzed as secondary endpoints. Results After PSM, 15 pairs of patients were selected for final analysis. Although the data failed to identify discrepancy in the remission rate of dysphagia between the two groups (73.3% VS 93.3%, P=0.33), the degree of dysphagia relief deviated significantly (2.13±0.52 VS 2.47±0.52, P=0.005). The onset of dysphagia remission was earlier in the combined treatment group than in the conventional treatment group (17.29±9.29 days VS 33.73±6.77 days, P<0.001). The median OS of conventional treatment group and combined treatment group were 21.10 months (95%CI 10.24∼31.96) and 36.67 months (95%CI 21.54∼51.80), respectively (P=0.048). The median PFS were 14.30 months (95%CI 7.79∼20.81) and 31.23 months (95%CI 13.68∼47.78), respectively (P=0.039). The rates of 1-year, 2-year and 3-year OS of conventional treatment and combined treatment group were 60%, 33.3%, 20% and 86.7%, 66.7%, 41.5%, respectively. The rates of 1-year, 2-year, and 3-year PFS of the two groups were 53.3%, 26.7%, 13.3% and 73.3%, 53.3%, 38.1%, respectively. The improvement of nutritional status in combined treatment group was better than that in conventional treatment group. The grade 3 toxicity rate was 46.7%, and no grade 4 or more toxicity was observed in all patients. The addition of PDT did not increase the risk of toxic reactions compared with concurrent chemoradiotherapy. Conclusion Photodynamic therapy sequential dose-reduction concurrent chemoradiotherapy can rapidly relieve dysphagia symptoms in patients with locally advanced obstructive EC. Compared with radical CCRT, it does not increase the incidence of treatment-related adverse reactions.

Medical images such as CT can provide important reference value for doctors to diagnose diseases. Identifying and segmenting lesions from medical images is crucial for its diagnosis and treatment. However, unlike other segmentation tasks, medical image has the characteristics of blurred boundaries and variable lesions sizes, which poses challenges to medical image segmentation. In this paper, we propose a Boundary-Guided Buffer Feedback Network(BGBF-Net), using the boundary guidance module to combine the low-level feature map rich in boundary information and the high-level semantic segmentation feature map generated by the encoder module, and output the features that focus on the boundary, which is used to enhance the attention of the decoder to boundary features. The buffer feedback module is used to strengthen the network’s supervision of the decoder while speeding up convergence of the model. We apply the proposed BGBF-Net on the LiTS dataset. Comprehensive results show that the BGBF-Net improves by 2.36% compared to other methods in terms of Dice.

Cervical cancer is a malignant tumor of the cervix in women. However, the pathogenesis of cervical cancer has not been fully understood. N6‐methyladenosine (m6A) is a kind of RNA modification that plays a critical role in cancer development. We aim to find out the possible m6A regulatory mechanism of the fat mass and obesity‐associated protein (FTO) on the development of cervical cancer. The proliferative capacity of cervical cancer cells was detected by 3‐(4,5‐dimethylthiazol‐2‐yl)−2,5‐diphenyl‐2H‐tetrazolium bromide (MTT), colony formation and 5‐ethynyl‐20‐deoxyuridine (EdU) staining. The migration and invasion of cervical cancer cells were determined by transwell assay. The function of FTO on tumor growth was evaluated by a xenograft model. We found that FTO was highly expressed in cervical cancer tissues and cell lines. FTO silencing suppressed the proliferation, migration, and invasion of cervical cancer cells. Mechanistically, FTO modulated the m6A modification of Zinc finger E‐box binding homeobox 1 (ZEB1) and Myelocytomatosis oncogene (Myc). Furthermore, ZEB1 and Myc overexpression reverse the effect of FTO knockdown on the malignant behaviors of cervical cancer cells. FTO may be a novel therapeutic target for cervical cancer.

Effects of miR-30a on cell cycle and apoptosis.

<p>Analysis of the effect of miR-30a on HP1γ protein and mRNA.</p>

Abstract Background Lipid droplet (LD) accumulation is a notable feature of obesity-induced cardiomyopathy; however, detailed processes governing cardiac LD content remains poorly understood. Reticulon 3 (RTN3), a tubular endoplasmic reticulum (ER) localized protein, was recently identified as a key modulator of lipid metabolism in adipocytes. But its role in cardiac lipid metabolism and the specific mechanism of RTN3 regulating lipid content are currently unknown. Purpose To investigate the role of RTN3 in cardiac LD accumulation and the mechanism by which RTN3 affects LD metabolism. Methods We labelled LD, free fatty acids (FFA), and nucleus in cardiomyocytes with fluorescent markers and upregulated/downregulated RTN3 expression with adenovirus. The effect of RTN3 on cardiac LD content and biogenesis was detected with confocal microscopy. Then we investigated the interaction partner of RTN3 with co-immunoprecipitation (Co-IP), liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis, and immunofluorescence staining. The function of the complex which RTN3 formed with its interaction protein was then explored. Results RTN3 overexpression significantly increased LD content in cardiomyocytes, which phenocopied the effects of palmitate stress. In contrast, palmitate-induced LD accumulation was blocked by RTN3 knockdown. Tubular ER, where RTN3 residents, is the primary organelle regulating LD biogenesis. Based on that, we hypothesized that the effect of RTN3 on LD content could be attributed to its direct effect on LD biogenesis in the ER. Further FFA tracing results demonstrated that RTN3 overexpression and palmitate could markedly increase FFA-LD colocalization, suggesting the LD biogenesis was activated, but this increase in colocalization was absent in cardiomyocytes infected with Ad sh-RTN3. Live cell imaging also revealed that upregulation of RTN3 significantly accelerated cardiac LD biogenesis and downregulation of RTN3 suppressed palmitate-induce LD biogenesis. Then we investigated the interaction partner of RTN3 and found that RTN3 formed a complex with fatty acids binding protein 5 (FABP5), which is an intracellular carrier for long-chain FFAs. Mechanistically, RTN3 directly bound with FABP5, which facilitated the directed transport of FFA to ER and thus promoted LD biogenesis. FABP5 knockdown blocked RTN3-mediated LD biogenesis. Moreover, we discovered that the 1st-194th amino acids of RTN3 was responsible for interacting with FABP5 and promoting LD biogenesis. Conclusions Our study reveals a novel mechanism contributing to LD biogenesis in cardiomyocytes. Based on our results, manipulating LD biogenesis by modulating RTN3 may be a potential strategy for treating LD accumulation in obese patients.RTN3 promoted lipid droplet biogenesisRTN3 formed a protein complex with FABP5

Background Hypertrophic scarring is the most serious and unmet challenge following burn and trauma injury and often leads to pain, itching and even loss of function. However, the demand for ideal scar prevention and treatment is difficult to satisfy. We aimed to discover the effects and mechanisms of adipose-derived stem cell (ADSC) exosomes in hypertrophic scarring.Methods ADSC exosomes were isolated from the culture supernatant of ADSCs and identified by nanoparticle tracking analysis, transmission electron microscopy and western blotting. The effect of ADSC exosomes on wound healing and scar formation was detected by the wound model of BALB/c mice. We isolated myofibroblasts from hypertrophic scar tissue and detected the cell viability, proliferation and migration of myofibroblasts. In addition, collagen formation and fibrosis-related molecules were also detected. To further disclose the mechanism of ADSC exosomes on fibrosis in myofibroblasts, we detected the expression of Smad2 in hypertrophic scar tissue and normal skin and the regulatory mechanism of ADSC exosomes on Smad2. Injection of bleomycin was performed in male BALB/c mice to establish an in vivo fibrosis model while ADSC exosomes were administered to observe their protective effect. The tissue injury of mice was observed via hematoxylin and eosin and Masson staining and related testing.Results In this study, we found that ADSC exosomes could not only speed up wound healing and improve healing quality but also prevent scar formation. ADSC exosomes inhibited expression of fibrosis-related molecules such as alpha-smooth muscle actin, collagen I (COL1) and COL3 and inhibited the transdifferentiation of myofibroblasts. In addition, we verified that Smad2 is highly expressed in both hypertrophic scar tissue and hypertrophic fibroblasts, while ADSC exosomes downregulated the expression of Smad2 in hypertrophic fibroblasts. Further regulatory mechanism analysis revealed that microRNA-125b-5p (miR-125b-5p) is highly expressed in ADSC exosomes and binds to the 3 ' untranslated region of Smad2, thus inhibiting its expression. In vivo experiments also revealed that ADSC exosomes could alleviate bleomycin-induced skin fibrosis and downregulate the expression of Smad2.Conclusions We found that ADSC exosomes could alleviate hypertrophic scars via the suppression of Smad2 by the specific delivery of miR-125b-5p.

Ferroptosis is a novel form of regulated cell death characterized by accumulated lipid reactive oxygen species (ROS) and inactivation of glutathione peroxidase 4 (GPX4). The present study aimed to investigate the role of microRNA (miRNA/miR)-15a in ferroptosis of prostate cancer cells. Bioinformatics analysis was performed to predict the potential interaction between miR-15a and the 3'-untranslated region (UTR) of GPX4 mRNA. The prostate cancer cell line, LNCAP was transfected with miR-15a mimics or small interfering (si)-GPX4. Reverse transcription-quantitative PCR and western blot analyses were performed to detect the mRNA and protein expression levels of GPX4, respectively. Biotin-RNA pull-down and dual-luciferase reporter assays were performed to verify the interaction between miR-15a and GPX4 mRNA. The Cell Counting Kit-8 assay was performed to assess cell proliferation, while lactate dehydrogenase (LDH) and intracellular ferrous iron levels were detected via ELISA. Lipid ROS and mitochondrial membrane potential (MMP) were assessed via flow cytometry and staining with C11-BIODIPY probes or JC-1. Furthermore, lipid peroxidation was identified by measuring malondialdehyde (MDA) levels. The results demonstrated that transfection with miR-15a mimics decreased GPX4 protein expression. Bioinformatics analysis revealed potential binding sites between miR-15a and the 3'-UTR region of GPX4, and RNA pull-down and the dual-luciferase reporter assays further confirmed the interaction between miR-15a and GPX4 mRNA. Both transfection with miR-15a mimics and si-GPX4 suppressed cell proliferation, elevated LDH release, accumulated intracellular ferrous iron and ROS, disrupted MMP and increased MDA levels. Taken together, the results of the present study suggest miR-15a induces ferroptosis by regulating GPX4 in prostate cancer cells, which provides evidence for investigating the therapeutic strategies of prostate cancer.

Background Angiogenesis provides essential nutrients and oxygen for tumor growth and has become the main mechanism of tumor invasion and metastasis. Exosomes are nanoscale membrane vesicles containing proteins, lipids, mRNA and microRNA (miRNA), which mediate intercellular communication and play an important role in tumor progression. Accumulated evidence indicates that tumor-derived exosomal miRNAs participate in the tumor microenvironment and promote angiogenesis. Methods Bioinformatic target prediction and dual luciferase reporter assays were performed to identify the binding site between miR-663b and the 3′-UTR of vinculin (VCL). VCL overexpression lentivirus and miR-663b overexpression/inhibition lentivirus were used to create a VCL overexpression model and miR-663b overexpression/inhibition model in-vitro. Immunohistochemistry (IHC) assays and western blot assays were used to detect protein expression. Exosome-cell cocultures, wound healing assays, tube formation assays and transwell assays were used to measure the migration and tube formation ability of vascular endothelial cells [human umbilical vein endothelial cells (HUVECs)]. siRNA targeted VCL was used to knockdown VCL. Results In the present study, we found that miR-663b was elevated in cervical cancer tissue and exosomes. miR-663b could bind the 3′-UTR of VCL and inhibit its expression. VCL is downregulated in cervical cancer, and decreased VCL has a negative correlation with a high level of miR-663b. Further studies demonstrated that exosomes secreted by cervical cancer cells can deliver miR-663b to HUVECs and inhibit the expression of VCL, thereby promoting angiogenesis and tumor growth. Conclusions miR-663b derived from cancer cell exosomes acts as a driving factor for angiogenesis and a potential target of antiangiogenic therapy in cervical cancer. Our findings illustrated a new signaling pathway, including exosomes, miRNAs and target genes, which provides potential targets for antiangiogenic therapy.

Abstract Background: Gastric cancer (GC) is still one major reason for cancer-related death worldwide and in China, which ranks the second highest common cancer death rate. It is of great importance to study the molecular mechanisms by which gastric cancer develops. Methods: In this study, in situ hybridization histochemistry (ISHH) was used to examine the lncRNA-GPAND expression levels using gastric cancer tissue array. The real-time live-cell imaging system was used to investigate the effect of GPAND on cell proliferation and apoptosis of GC cell lines. Cell cycle of AGS cell line was examined after GPAND was suppressed using the flow cytometry (FCM). Transwell method was used to study the effect of GPAND on the invasion characteristics of GC cell line. Then the next generation sequencing (NGS) was used to study the potential molecular mechanism and the pathway, and the RT-qPCR was performed to verify the potential targets found by NGS method. Results: It was shown that GPAND was significantly over-expressed in the gastric cancer (GC) tissues (n=215) compared with the paired non-cancerous tissues (n=215), the expression levels of GPAND of GC tissues of TNM stage I-II (n=45) were significantly higher than that of stage III-IV (n=147). It has shown that knockdown of GPAND inhibited the AGS and N87 cell proliferation and promoted the cell apoptosis of AGS and N87 cell lines significantly, and the G1 phase percentage was remarkably increased in GPAND knockdown group of AGS cell line compared with control group. Moreover, suppression of GPAND inhibited the AGS cell invasion significantly. It was found via the NGS method that RUNX2 and MMP13 were significantly up-regulated when the GPAND was over-expressed. Conclusions: These observations suggest the lncRNA-GPAND/RUNX2/MMP13 axis to be a viable therapeutic target for gastric cancer.

Expression of the immunoglobulin superfamily member CD155 was increased in a variety of human malignancies, but the role of CD155 in tumorigenesis and tumor development in cervical cancer has not been elucidated. In this study, immunohistochemistry and enzyme-linked immunosorbent assay analyses showed that CD155 expression gradually increases with the degree of cervical lesions. In vitro and in vivo, reducing the expression of CD155 inhibited cell proliferation, cell viability and tumor formation and arrested the cell cycle in G0/G1 phase. Antibody array-based profiling of protein phosphorylation revealed that CD155 knockdown can inhibited the AKT/mTOR/NF-κB pathway and activated autophagy and apoptosis; the opposite effects were observed upon CD155 has overexpression. We proved that there is an interaction between CD155 and AKT by immunoprecipitation. We further confirmed the mechanism between CD155 and AKT/mTOR/NF-κB through rescue experiments. AKT knockdown reversed the anti-apoptotic effects and activation of the AKT/mTOR/NF-κB pathway induced by CD155 overexpression. Our research demonstrated that CD155 can interact with AKT to form a complex, activates the AKT/mTOR/NF-κB pathway and inhibit autophagy and apoptosis. Thus, CD155 is a potential screening and therapeutic biomarker for cervical cancer.

Background Circular RNAs (circRNAs), a new type of non-coding RNA, have been demonstrated to play critical roles in the progression of various of malignant cancers. In the present study, we identified a circRNA termed as circTADA2A which was hypothesized that may be significantly up-regulated in OC tissues and cell lines. Results The results revealed that ectopic expression of circTADA2A promoted the cell proliferation, migration, invasion and colony formation ability of OC cells. Constantly, silencing of circTADA2A inhibited those of OC cells. Furthermore, we identified that circTADA2A was able to target miR-203 in OC cell. MiR-203 was able to reverse the oncogenic effect of circTADA2A on proliferation, migration and metastasis of OC cells through targeting SMAD1 . Conclusions We reported that circTADA2A served as a competing endogenous RNA (ceRNA) to sponge miR-203 and blocked its regulation of SMAD1 . These findings provide insights into OC progression and also potential new targets for diagnose or treatment of OC.

Transforming growth factor (TGF)-β1 is a key cytokine affecting the pathogenesis and progression of cervical cancer. Tumor-derived exosomes contain microRNAs (miRNAs/miRs) that interact with cancer and stromal cells, thereby contributing to tissue remodeling in the tumor microenvironment (TME). The present study was designed to clarify how TGF-β1 affects tumor biological functions through exosomes released by cervical cancer cells. Deep RNA sequencing found that TGF-β1 stimulated cervical cancer cells to secrete more miR-663b-containing exosomes, which could be transferred into new target cells to promote metastasis. Further studies have shown that miR-663b directly targets the 3′-untranslated regions (3′-UTR) of mannoside acetylglucosaminyltransferase 3 (MGAT3) and is involved in the epithelial-mesenchymal transition (EMT) process. Remarkably, the overexpression of MGAT3 suppressed cervical cancer cell metastasis promoted by exosomal miR-663b, causing increased expression of epithelial differentiation marker E-cadherin and decreased expression of mesenchymal markers N-cadherin and β-catenin. Throughout our study, online bioinformation tools and dual luciferase reporter assay were applied to identify MGAT3 as a novel direct target of miR-663b. Exosome PKH67-labeling experiment verified that exosomal miR-663b could be endocytosed by cervical cancer cells and subsequently influence its migration and invasion functions which were measured by wound healing and Transwell assays. The expression of miR-663b and MGAT3 and the regulation of the EMT pathway caused by MGAT3 were detected by quantitative real-time transcription-polymerase chain reaction (qPCR) and western blot analysis. These results, thus, provide evidence that cancer cell-derived exosomal miR-663b is endocytosed by cervical cancer cells adjacent or distant after TGF-β1 exposure and inhibits the expression of MGAT3, thereby accelerating the EMT process and ultimately promoting local and distant metastasis.

Prostate cancer (PCa) remains a leading cause of mortality among men in the United States and Western Europe. The molecular mechanism of PCa pathogenesis has not been fully elucidated. In the present study, the expression profile of E2F transcription factor 7 (E2F7) in PCa was examined using immunohistochemistry and reverse transcription-quantitative PCR, whilst cell cycle progression and apoptosis were determined using fluorescent cell activated sorting techniques. Cell viability was measured using Cell Counting Kit-8 in loss- and gain-of-function studies. Dual-luciferase reporter assay was used to verify if E2F7 was one of the potential targets of miR-30c. The staining score of E2F7 of PCa tissues was found to be notably higher compared with that of adjacent normal tissues. Suppression of E2F7 expression in PCa cell lines led to significantly reduced proliferation rates, increased proportion of cells in the G(1)phase of the cell cycle and higher apoptotic rates compared with those in negative control groups. Dual-luciferase reporter assay revealed E2F7 to be one of the binding targets of microRNA (miR)-30c. In addition, transfection of miR-30c mimics into PCa cells resulted in reduced cell viability, increased proportion of cells in the G(1)phase and higher apoptotic rates. By contrast, transfection with the miR-30c inhibitor led to lower apoptosis rates of PCa cells compared with negative control groups, whilst E2F7 siRNA co-transfection reversed stimulatory effects of miR-30c inhibitors on cell viability. In addition, the expression of cyclin-dependent kinase inhibitor p21 were found to be upregulated by transfection with either E2F7 siRNA or miR-30c mimics into PCa cells. In conclusion, the present study suggested that E2F7 may be positively associated with PCa cell proliferation by inhibiting p21, whereas E2F7 is in turn under regulation by miR-30c. These observations suggest the miR-30c/E2F7/p21 axis to be a viable therapeutic target for PCa.

The incidence and mortality rates of cancer have been increasing in developing countries, particularly in Asia. Therefore to provide optimal comprehensive care to the cancer patients, the care plan must focus on the comprehensive needs of cancer patients. The purpose of this study was to investigate the comprehensive needs of cancer patients, and explore the associated factors. In a cross-sectional questionnaire study, a total of 200 cancer patient-caregiver dyads were selected and interviewed in Mainland China by convenient sampling method. Patients’ comprehensive needs were assessed with Comprehensive Needs Assessment Tool in cancer for Patients (CNAT), including seven domains (Information, Psychological Problems, Health Care Staffs, Physical Symptoms, Hospital Facilities and Services, Social/Religious/Spiritual Support and Practical Support). Both cancer patients and caregivers completed the sociodemographic survey. The mean differences in domain scores for different characteristics groups were compared by one-way ANOVA or non-parametric analyses, and influencing factors defined with multivariate regression analysis. The cancer patients’ need for Health Care Staffs (78.35 ± 13.08) was the highest among the seven domains, followed by the need for Information (71.18 ± 17.39) and the need for Hospital Facilities and Services (52.65 ± 13.35). The lowest score was the need for Physical Symptoms (35.12 ± 16.68). Patients who were female, with low family monthly income, at their own expense, and with highly educated caregivers had higher score of CNAT. Also sociodemographic characteristics were associated with each domain need of cancer patients. This study shows that cancer patients experience high levels of needs for health-care staff and information, and the different needs are closely related to their sociological characteristics. The provision of health care can be adapted to meet the different needs of cancer patients of different epidemiological characteristics at different times during the course of treatment.

Recent research suggested that microRNA 96 (miR-96) might function as an oncogene in several types of cancers. Therefore, the purpose of this study was to probe into the mechanism of miR-96 in hepatocellular carcinoma (HCC) cells. HCC tissues and non-tumorous tissues, HCC cell lines, and healthy cell lines were all involved in this study. Quantitative real-time PCR (qRT-PCR) and Western blot were used to detect miR-96 and SOX6 mRNA and protein expressions. The direct regulation of miR96 on SOX6 was confirmed by luciferase reporter assays. Cell proliferation and growth were determined by MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay and colony formation assay. Wound healing and transwell assay were employed for migration and invasion analyses. Finally, SPSS 21.0 and GraphPad 7.0 were applied for statistical analyses. In HCC tissues, miR-96 was highly expressed while SOX6 was lowly expressed. The overexpression of miR-96 reversely inhibited the expression of SOX6, contributing to the promotion of the biological functions of HCC cells. miR-96 could promote cell proliferation, migration, and invasion in HCC by targeting SOX6.

OBJECTIVE:This study aimed to evaluate the prognosis significance of zinc-finger E-box binding homeobox 2 (ZEB2) and transforming growth factor β1 (TGF-β1) as well as other clinical characteristics in epithelial ovarian cancer (EOC). METHODS:This retrospective study examined the expressions of ZEB2 and TGF-β1 in 64 EOC specimens, 36 benign ovarian tumor specimens, and 28 normal ovarian specimens by immunohistochemistry. The correlation of the expressions of ZEB2 and TGF-β1 was analyzed by the Spearman rank correlation analysis. The Kaplan-Meier method was used to construct crude survival curves, and the prognostic roles of ZEB2 and TGF-β1 as well as clinical characteristics were evaluated by Cox proportional hazards regression analysis. RESULTS:The positive expression rates of ZEB2 and TGF-β1 were increased in EOC specimens compared with benign ovarian tumor and normal ovary specimens (P < 0.05), and ZEB2 expression was positively correlated with TGF-β1 expression (r = 0.538, P = 0.000). In addition, the overall survival rate of EOC patients was associated with the expressions of ZEB2 and TGF-β1, age, differentiated grade, International Federation of Gynecology and Obstetrics (FIGO) stage, preoperative serum CA125 level, postoperative start time of chemotherapy, and treatment course (all P < 0.05). Multivariate Cox regression demonstrated that FIGO stage (P = 0.033), TGF-β1 expression (P = 0.043), postoperative start time of chemotherapy (P = 0.009), and treatment course (P = 0.000) were prognostic factors for EOC. CONCLUSIONS:ZEB2 and TGF-β1 may promote EOC progression, and FIGO stage, TGF-β1 expression, postoperative start time of chemotherapy, and treatment course may be associated with the prognosis of EOC.

ObjectiveTo compare the natural fertility outcomes of salpingotomy and salpingectomy among women treated for tubal pregnancy.MethodsAn online database search including PubMed, Embase, CENTRAL and Web of Science was performed to identify studies comparing salpingotomy and salpingectomy to treat women with tubal pregnancy. The search included papers published after the databases were established until May 2015. Two reviewers independently screened literature according to the inclusion and exclusion criteria and then extracted data and assessed the methodological quality of all of the included studies. The meta-analysis was conducted using RevMan 5.3 software. The registration number is CRD42015017545 in PROSPERO.ResultsTwo randomized controlled trials (RCTs) and eight cohort studies, including a total of 1,229 patients, were znalyzed. The meta-analysis of the RCT subgroup indicated that there was no statistically significant difference in IUP rates (RR = 1.04, 95% CI = 0.89-1.21, P = 0.61) nor the repeat ectopic pregnancy (REP) rate (RR = 1.30, 95% CI = 0.72-2.38, P = 0.39) between the salpingotomy and salpingectomy group. In contrast, the cohort study subgroup analysis revealed that the IUP rate was higher in the salpingotomy group compared with the salpingectomy group (RR = 1.24, 95% CI = 1.08-1.42, P = 0.002); Salpingotomy also increased the risk of REP rate (RR = 2.27, 95% CI = 1.12-4.58, P = 0.02). The persistent ectopic pregnancy (PEP) occurred more frequently in the salpingotomy group than the salpingectomy group (RR = 11.61, 95% CI = 3.17-42.46, P = 0.0002). An IUP would be more likely to occur after salpingotomy than salpingectomy when the follow-up time was more than 36 months (RR = 1.16, 95% CI = 1.02-1.32, P = 0.03). The IUP rate (RR = 1.13, 95% CI = 1.01-1.26, P = 0.03), and the REP rate (RR = 1.62, 95% CI = 1.02- 2.56, P = 0.04) was higher after salpingotomy than salpingectomy among patients from Europe compared with those from America.ConclusionsBased on the available evidence, we believe that for patients with a healthy contralateral tube operated for tubal pregnancy, the subsequent fertility after salpingectomy and salpingotomy are similar in the long term. The fertility prospects will not be improved via salpingotomy compared with salpingectomy.