Retrospective analysis of robot-assisted laparoscopic transabdominal anterior approach for the treatment of lumbar paravertebral schwannoma.

BACKGROUND: The main objective of this study was to investigate the impact of robot-assisted laparoscopic resection on paravertebral tumours using the anterior peritoneal approach. METHODS: A retrospective analysis to identify patients with paravertebral tumours. A total of 21 patients, who underwent robot-assisted laparoscopic transabdominal anterior approach surgery from March 2012 to August 2020. RESULTS: The median operation time was 66.2 ± 14.5 min, with a range of 0-100 min. Intraoperative blood loss was minimal, with a median of 11.4 ± 7.9 mL and a range of 5-30 mL. The median tumour length was 4.8 ± 2.3 cm, ranging from 2.1 to 11.3 cm. Postoperative hospitalisation lasted for a median of 3.2 ± 0.9 days. During the 48-month follow-up period, no tumour recurrence or residual was observed in any patient. CONCLUSIONS: Robot-assisted laparoscopic resection of lumbar paravertebral schwannoma proved to be a safe and viable surgical approach. It offers a relatively new treatment option for paraspinal schwannoma.

Single-position robot-assisted versus laparoscopic antegrade bilateral inguinal lymphadenectomy for penile cancer: A retrospective controlled study.

OBJECTIVES: The main purpose of this study was to compare the surgical strategy and clinical outcomes of single-position robotic assisted laparoscopic anterograde bilateral inguinal lymphadenectomy for penile cancer. MATERIALS AND METHODS: 21 patients were diagnosis with squamous cell carcinoma and identified from March 2010 to December 2020 in our department. Ten patients were received single-position robotic assisted laparoscopic anterograde bilateral inguinal lymphadenectomy (robot-assisted group), and eleven patients underwent laparoscopic inguinal lymphadenectomy (laparoscopic group). Preoperative physical examination and related auxiliary examinations all indicated bilateral inguinal lymph node enlargement, and there was no distant metastasis patient presented during the follow-up period. RESULTS: There was no intraoperative conversion to open surgery. The operation time under robot-assisted group was 104 ± 13 min which was significantly shorter than laparoscopic group (136 ± 11 min, P < 0.01). The average number of lymph nodes was 22.2 ± 4.5 of both sides in robot-assisted group, which was statistically different compared with laparoscopic group (15.4 ± 3.1, p < 0.01). Moreover, there was significant difference of hospitalization cost between two groups (CNY 67429 ± 5586 vs 28582 ± 3774, P < 0.01). No differences in operation time, blood loss, and length of stay were recorded. CONCLUSIONS: The single-position robotic assisted laparoscopic anterograde bilateral inguinal lymphadenectomy reveals with shorter operating time, and better surgical effect, Moreover, we prefer to no change the trocars layout and mechanical arm system during the operation.

TLR3 Serves as a Prognostic Biomarker and Associates with Immune Infiltration in the Renal Clear Cell Carcinoma Microenvironment.

BACKGROUND: Clear cell renal cancer (KIRC) is one of the most common cancers globally, with a poor prognosis. TLRs play a vital role in anticancer immunity and the regulation of the biological progress of tumour cells. However, the precise role of TLRs in KIRC is still ambiguous. METHODS: Various bioinformatics analysis and clinical validation of tissues were performed to evaluate the prognostic value of TLRs and their correlation with immune infiltration in KIRC. RESULTS: The expression of TLR2/3/7/8 was increased at both mRNA and protein levels in KIRC. TLRs in KIRC were involved in the activation of apoptosis, EMT, RAS/MAPK, and RTK pathways, as well as the inhibition of the cell cycle and the hormone AR pathway. Drug sensitivity analysis revealed that high expression of TLR3 and low expression of TLR7/9/10 were resistant to most of the small molecules or drugs from CTRP. Enrichment analyses showed that TLRs were mainly involved in innate immune response, toll-like receptor signalling pathway, NF-kappa B signalling pathway, and TNF signalling pathway. Furthermore, a high-level TLR3 expression was associated with a favourable prognosis in KIRC. Validation research further confirmed that TLR3 expression was increased in KIRC tissues, and high TLR3 levels were associated with poor overall survival. Moreover, TLR3 in KIRC showed a positive association with an abundance of immune cells, including B-cells, CD4+ T-cells, CD8+ T-cells, macrophage, neutrophils, and dendritic cells, and the expression of the immune biomarker sets. Several TLR3-associated kinase, miRNA, or transcription factor targets were also identified in KIRC. CONCLUSION: Our results indicate that TLR3 serves as a prognostic biomarker and associated with immune infiltration in KIRC. This work lays a foundation for further studies on the role of TLR3 in the carcinogenesis and progression of KIRC.

Reconstruction of full-length ureter defects by laparoscopic bladder flap forming.

To evaluate the safety and efficacy of laparoscopic bladder muscle flap reconstruction in the treatment of extensive ureteral avulsion. Patients with full-length (re length > 20 cm) and upper ureteral (avulsion length > 10 cm) defects were eligible. All patients were treated with laparoscopic bladder muscle flap reconstruction. Peri-operative information and post-operative complications were recorded. The kidney function, urinary ultrasound or computed tomography (CT), sun-renal function tests emission computed tomography (ECT) and cystography after operation were recorded. Ten patients were included (7 with full-length and 3 with upper ureteral defects). Median age was 56 years and 70% of them were female. The average operation time and blood loss was 124 min and 92.2 ml. There was no treatment-related adverse effects including urinary leakage, renal colic, fever, etc. The median follow-up was 18.5 months (3-39 months). The surgery did not significantly alter the renal function and separation degree of the renal pelvis during long-term follow-up. Double J stents were removed in nine patients (90%) within six months after operation. Only one case was diagnosed with post-operative anastomotic stricture, and subsequently received laparoscopic ipsilateral nephrectomy one year after the reconstruction operation. All cases had normal voiding and pear-shaped cystography. Laparoscopic bladder flap repair is a safe and effective treatment approach together with several advantages for patients with full-length or upper ureteral avulsion.

Mining TCGA database for tumor mutation burden and their clinical significance in bladder cancer.

BACKGROUND: Bladder cancer is the ninth most-common cancer worldwide and it is associated with high morbidity and mortality. Tumor mutational burden (TMB) is an emerging biomarker in cancer characterized by microsatellite instability. TMB has been described as a powerful predictor of tumor behavior and response to immunotherapy. METHODS: A total of 443 bladder cancer samples obtained from The Cancer Genome Atlas (TCGA) were analyzed for mutation types, TMB values, and prognostic value of TMB. Differentially expressed genes (DEGs) were identified from the TMB groupings. Functional analysis was performed to assess the prognostic value of the first 30 core genes. CIBERSORT algorithm was used to determine the correlation between the immune cells and TMB subtypes. RESULTS: Single nucleotide polymorphism (SNP) and C>T were reported as the most common missense mutations and we also identified a high rate of mutations in TP53, TTN, KMT2D. Bladder cancer patients with high TMB showed a better prognosis. Enrichment analysis of the DEGs revealed that they were involved in the regulation of the P13K-Akt signaling pathway, cytokine-cytokine receptor interaction, and Ras signaling pathway. The high expression of hub genes ADRA2A, CXCL12, S1PR1, ADAMTS9, F13A1, and SPON1 was correlated with poor overall survival. Besides, significant differences in the composition of the immune cells of T cells CD8, T cells CD4 memory activated, NK cells resting and Mast cells resting were observed. CONCLUSIONS: The present study provides a comprehensive and systematic analysis of the prediction of TMB in bladder cancer and its clinical significance. Also, the study provides additional prognostic information and opportunities for immunotherapy in bladder cancer.

Overexpressed miR-122-5p Promotes Cell Viability, Proliferation, Migration And Glycolysis Of Renal Cancer By Negatively Regulating PKM2.

OBJECTIVE: Renal cancer is one of the most deadly urological malignancies. Currently, there is still a lack of effective treatment. Our purpose was to explore the mechanisms of miR-122-5p in renal cancer. METHODS: The expression levels of miR-122-5p and pyruvate kinase M2 (PKM2) in renal cancer cells were detected by RT-qPCR and Western blot analyses, respectively. Then, we measured the cell viability after knockdown of miR-122-5p and PKM2 using CCK-8 assay. Moreover, flow cytometry was used to investigate cell cycle and apoptosis of renal cancer cells. The cell migration of renal cancer cells transfected by miR-122-5p inhibitor and siPKM2 was then detected by wound healing assay. Furthermore, glucose consumption and lactate production were measured. Autophagy-related protein LCII/I was detected by Western blot. RESULTS: MiR-122-5p was upregulated in renal cancer cells compared to HK2 cells, especially in 786-O cells. We found that silencing miR-122-5p promoted PKM2 expression in 786-O cells. After transfection of siPKM2 or miR-122-5p inhibitor, the cell viability of 786-O cells was significantly reduced. Furthermore, the G1 phase of 786-O cells was significantly blocked, and the S phase was significantly increased. In addition, knockdown of miR-122-5p or PKM2 promoted renal cancer cell apoptosis and inhibited cell migration. Glucose consumption of 786-O cells was significantly increased after transfection by siPKM2. Silencing miR-122-5p significantly promoted the expression levels of LCII/I. CONCLUSION: Our findings revealed that overexpressed miR-122-5p promotes renal cancer cell viability, proliferation, migration, glycolysis and autophagy by negatively regulating PKM2, which provide a new insight for the development of renal cancer therapy.

Jarid2 enhances the progression of bladder cancer through regulating PTEN/AKT signaling.

AIMS: Jumonji AT-rich interactive domain 2 (Jarid2) is an interacting component of PRC2 which catalyzes methylation of H3K27 (H3K27me3) and causes the downregulation of PTEN. In the present study, we aimed to explore whether Jarid2 could interact with H3K27me3 to regulate PTEN expression in bladder cancer. MAIN METHODS: Jarid2 expression in bladder cancer tissues and cells were determined by western blotting and RT-PCR. CCK-8, flow cytometry, transwell chamber and in vivo xenograft assays were performed to assess cell growth, apoptosis, migration and tumorigenesis, respectively. Chromatin immunoprecipitation (ChIP) assay was used to assess the methylation of PTEN. KEY FINDINGS: Jarid2 expression was increased in bladder cancer tissues and cells. Downregulation of Jarid2 with shRNA transfection obviously inhibited the proliferation, migration and tumorigenesis of bladder cancer T24 and HT-1376 cells and induced cell apoptosis. Jarid2 downregulation decreased the expression of p-AKT and increased PTEN expression. Besides, Jarid2 down-regulation repressed the epithelial-mesenchymal transition (EMT), whereas knockdown of PTEN impaired this effect. Moreover, upregulation of Jarid2 increased the combination of PTEN promoter and H3K27me3, and 5-aza-CdR rescued it. Meanwhile, 5-aza-CdR administration abolished Jarid2 roles in the promotion of EMT process and AKT activation, as well as the reduction of PTEN expression. SIGNIFICANCE: Overall, the present study elaborated that Jarid2 facilitated the progression of bladder cancer through H3K27me3-mediated PTEN downregulation and AKT activation, which might provide a new mechanism for Jarid2 in promoting bladder cancer progression.

Correction: Up-regulation of p16 by miR-877-3p inhibits proliferation of bladder cancer.

[This corrects the article DOI: 10.18632/oncotarget.10575.].

Diagnostic performance of PCA3 and hK2 in combination with serum PSA for prostate cancer.

OBJECTIVES: The prostate cancer gene 3 (PCA3), human kallikrein 2, and miRNA-141 are promising prostate cancer (Pca) specific biomarkers. Our aim was to evaluate the detection of PCA3, human glandular kallikrein 2 (hk2), and miRNA-141 mRNA in peripheral blood of patients received prostate biopsy. What's more, we want to detect the value of combination of PSA (prostate specific antigen) in the early diagnosis of PCa. MATERIALS AND METHODS: Hundred patients were divided into 2 groups according to the results of pathologic diagnosis. Quantitative real-time PCR (qRT-PCR) was used to evaluate the mRNA of PCA3, hk2, and miRNA-141 in peripheral blood. At the same time, analyze those clinical outcomes used in the patients. We compared these different outcomes to evaluate the value of new molecular markers. RESULTS: The level of mRNA of PCA3, hK2, and miR-141 in Pca group were significantly higher than that in BPH. PSA had the highest sensitivity in predicting Pca diagnosis (76.7%); PCA3 had the highest specificity (82.5%). And the combination of PCA3, PSA, and hK2 improved area under the curve (AUC)-receiver operating characteristic (ROC) curve largely, especially those with PSA 4-10ng/mL. CONCLUSIONS: PCA3, hK2, and miRNA-141 were biomarkers of Pca with potential clinical application value, especially in patients with PSA gray area. Combining PCA3, PSA, and hK2 performed better than individual biomarkers alone in predicting Pca.

Milk/dairy products consumption and gastric cancer: an update meta-analysis of epidemiological studies.

The relationship between dairy consumption and gastric cancer risk has not been well studied. We therefore performed a update meta-analysis to evaluate the relationship. Published cohort and case-control studies were identified via computer searches and reviewing the reference lists of the key articles. Random effects meta-analysis was used to pool effects from 5 cohort and 29 case-control studies. The odds ratio for the overall association between dairy consumption and gastric cancer was 1.20 (95%confidence interval: 1.04-1.39). The combined risk estimate was similar for population-based case-control studies (odds ratio = 1.27, 95%confidence interval: 1.00-1.61), but was reduced for hospital-based studies (odds ratio = 1.22; 95%confidence interval: 0.95-1.57) and cohort studies (odds ratio = 0.99; 95%confidence interval: 0.77-1.28). There was high heterogeneity in overall analyses. In the population-based subgroup analyses, the odds ratio was 0.96 (95%confidence interval: 0.69-1.34) when considering five studies assessing exposure two or more years before interview, and the association strengthened (odds ratio = 1.91, 95%confidence interval: 1.60-2.28) when dairy consumption was evaluated one year or less prior to interview. In conclusion, we found adverse effect of dairy consumption associated with gastric cancer.

c-Met, CREB1 and EGFR are involved in miR-493-5p inhibition of EMT via AKT/GSK-3ß/Snail signaling in prostate cancer.

miR-493-5p downregulation has emerged as a critical player in cancer progression yet, the underlying mechanisms of miR-493-5p expression pattern and its function in prostate cancer remains to be elucidated. Here, we illustrate that miR-493-5p is frequently downregulated in prostate cancer, at least partially due to altered DNA methylation. miR-493-5p functions as a tumor suppressor in prostate cancer cells. c-Met, CREB1 and EGFR are downstream target genes of miR-493-5p. miR-493-5p inhibits EMT via AKT/GSK-3ß/Snail signaling in prostate cancer. Taken together, our study identified c-Met, CREB1, EGFR and miR-493-5p establish a regulatory loop in prostate cancer, which could prove useful in the development of effective and therapies against prostate cancer.

MicroRNA-608 inhibits proliferation of bladder cancer via AKT/FOXO3a signaling pathway.

BACKGROUND: Current evidence indicates that miR-608 is widely down-regulated in various malignant tumors including liver cancer, colon cancer, lung cancer and glioma, and acts as a tumor suppressor by inhibiting cell proliferation, invasion and migration or by promoting apoptosis. The specific biological function of miR-608 in bladder cancer is still unknown. METHODS: qRT-PCR and Chromogenic in Situ Hybridization (CISH) was conducted to assess the expression of miR-608 in paired BCa tissues and adjacent non-tumor bladder urothelial tissues. Bisulfite sequencing PCR was used for DNA methylation analysis. CCK-8, colony formation and flow cytometry assays were performed, and a xenograft model was studied. Immunohistochemistry staining was performed with peroxidase and DAB. The target of miR-608 was validated with a dual-luciferase reporter assay, quantitative RT-PCR, and Western blotting. RESULTS: miR-608 is frequently down-regulated in human BCa tissues. The methylation status of CpG islands is involved in the regulation of miR-608 expression. Overexpression of miR-608 inhibits the proliferation and tumorigenesis of BCa cells in vitro and in vivo. Additionally, up-regulation of miR-608 in BCa cells induces G1-phase arrest through AKT/FOXO3a signaling. In contrast, down-regulation of miR-608 promotes proliferation and cell cycle progression in BCa cells. Moreover, the expression of FLOT1 was directly inhibited by miR-608, the down-regulation of FLOT1 induced by siFLOT1 could be significantly reversed by miR-608 inhibitor. Similarly, the up-regulation of FLOT1 by FLOT1 overexpression plasmid (pFLOT1) could also reverse the suppressed cell proliferation caused by miR-608. CONCLUSIONS: miR-608 is a potential tumor suppressor in BCa, and the restoration of miR-608 might be a promising therapeutic option for BCa.

miR-148a-3p represses proliferation and EMT by establishing regulatory circuits between ERBB3/AKT2/c-myc and DNMT1 in bladder cancer.

miR-148a-3p downregulation has emerged as a critical factor in cancer progression yet, the underlying mechanisms of miR-148a-3p expression pattern and its function in bladder cancer remains to be elucidated. Here, we illustrate that miR-148a-3p is frequently downregulated in bladder cancer and that its expression may be regulated by DNA methylation. DNA methyltransferase 1 (DNMT1) and miR-148a-3p function in a positive feedback loop in bladder cancer. miR-148a-3p overexpression functions as a tumor suppressor in bladder cancer cells. miR-148a-3p inhibits bladder cancer cell proliferation and epithelial-mesenchymal transition (EMT) by regulating ERBB3/AKT2/c-myc and ERBB3/AKT2/Snail signaling. ERBB3, DNMT1 and AKT2 are downstream miR-148a-3p target genes. Furthermore, the miR-148a-3p/ERBB3/AKT2/c-myc signaling axis establishes a positive feedback loop in the regulation of bladder cancer. Taken together, our study demonstrates novel regulatory circuits involving miR-148a-3p/ERBB3/AKT2/c-myc and DNMT1 that controls bladder cancer progression, which may be useful in the development of more effective therapies against bladder cancer.

Pesticide exposure and risk of bladder cancer: A meta-analysis.

OBJECTIVE: We conducted a meta-analysis to quantitatively evaluate the correlation between pesticide exposure and the risk of bladder cancer by summarizing the results of published case-control and cohort studies. METHODS: A systematic literature search of articles update to February 2015 was conducted via Pubmed, Web of Science, Cochrane Library, and the Chinese National Knowledge Infrastructure (CNKI) databases, and the references of the retrieved articles. Fixed- or random-effect models were used to summarize the estimates of OR with 95% CIs for the highest versus the lowest exposure of pesticide. RESULTS: The pooled OR estimates indicated that pesticide exposure was associated with an increased risk of bladder cancer (OR=1.649, 95% CI 1.223-2.223). In subgroup analysis, we detected pesticide exposure demonstrated as a significant risk factor on bladder cancer in America (OR=1.741, 95% CI 1.270-2.388). Similar results were discovered in both case-control group and cohort group (OR=2.075, 95% CI 1.183-3.638, OR=1.146, 95% CI 1.074-1.223, respectively). No evidence of publication bias was found by Begg's or Egger's test (P = 0.210, P = 0.358, respectively). CONCLUSION: In conclusion, our meta-analysis indicated that pesticide exposure was associated with an increased risk of bladder cancer. Further researches should be conducted to confirm the findings in our study and better clarify the potential biological mechanisms.

Hypertension and risk of prostate cancer: a systematic review and meta-analysis.

The previously reported association between hypertension and prostate cancer risk was controversial. We performed this systematic review and meta-analysis of all available studies to summarize evidence on this association. Studies were identified by searching PubMed, Web of Science and Chinese National Knowledge Infrastructure (CNKI) databases through January 2016. Pooled relative risks (RRs) with their corresponding 95% confidence intervals (CIs) were calculated using a random-effects model. A total of 21 published studies were included in this meta-analysis. A significant increase in the risk of prostate cancer (RR 1.08, 95% CI 1.02-1.15, P = 0.014) was observed among individuals with hypertension. There was statistically significant heterogeneity among included studies (P < 0.001 for heterogeneity, I(2) = 72.1%). No obvious evidence of significant publication bias was detected by either Begg's test (P = 0.174) or Egger's test (P = 0.277). In conclusion, this meta-analysis indicates that hypertension may be associated with an increased risk of prostate cancer. Considering the substantial heterogeneity and residual confounding among included studies, further large-scale, well-designed prospective cohorts, as well as mechanistic studies, are urgently needed to confirm our preliminary findings.

Up-regulation of p16 by miR-877-3p inhibits proliferation of bladder cancer.

Despite the recent studies which have shown that microRNA (miRNA) negatively regulates gene expression by silencing the expression of target genes, here we reported the new evidence of microRNA-mediated gene activation by targeting specific promoter sites. We identified a miR-877-3p binding site on the promoter site of tumor suppressor gene p16 which alters frequently in bladder cancer. Enforced expression of miR-877-3p could increase the expression of p16, which inhibit the proliferation and tumorigenicity of bladder cancer through cell cycle G1-phase arrest. Further evidences confirmed that the correlation between p16 activation and miR-877-3p was due to the direct binding. These findings demonstrate the anti-tumor function of miR-877-3p in bladder cancer cells and reveal a new pattern of miRNA involved gene regulation.

Is magnetic resonance/ultrasound fusion prostate biopsy better than systematic prostate biopsy? An updated meta- and trial sequential analysis.

We systematically reviewed the literature to determine whether Magnetic Resonance/Ultrasound (MR/US) fusion prostate biopsy is better than systematic biopsy for making a definitive diagnosis of prostate cancer. The two strategies were also compared for their ability to detect lesions with different degrees of suspicion on MRI and clinically significant prostate cancer, and the number of cores needed for diagnosis. The Cochrane Library, Embase, Web of Knowledge, and Medline were searched from inception until May 1, 2015. Meta-analysis was conducted via RevMan 5.2 software. Data was expressed as risk ratio (RR) and 95% confidence interval. Trial sequential analysis was used to assess risk of random errors. Fourteen trials were included, encompassing a total of 3105 participants. We found that MR/US fusion biopsy detected more prostate cancers than systematic biopsy (46.9% vs. 44.2%, p=0.03). In men with moderate/high MRI suspicion, MR/US fusion biopsy did better than systematic biopsy (RR = 1.46; p < 0.05) for making a diagnosis. Moreover, MR/US fusion biopsy detected more clinically significant cancers than systematic biopsy (RR = 1.19; p < 0.05). We recommend that MR/US fusion prostate biopsy be used to better detect prostate cancer, particularly in patients with moderate/high suspicion lesions on MRI.

MicroRNA-195-5p, a new regulator of Fra-1, suppresses the migration and invasion of prostate cancer cells.

BACKGROUND: An increasing number of studies have demonstrated that deregulation of microRNAs (miRNAs) was a common event in tumor tissues and miRNAs would be treated as ideal tumor biomarkers or therapeutic targets. miR-195-5p (termed as miR-195 for briefly in the following part) was suggested to function as a tumor suppressor in cancer development and progression. However, the roles of miR-195 in human prostate cancer are still elusive. Thus, this study was performed to investigate the biological functions and its molecular mechanisms of miR-195 in human prostate cancer cell lines, discussing whether it has a potential to be a therapeutic way of prostate cancer. METHODS: Two human prostate cancer cell lines were analyzed for the expression of miR-195 by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR). A gain-of-function study of miR-195 was conducted by transfecting mimics into DU145 and PC3 cells and cell motility and invasion ability were evaluated by wound healing assay and transwell assay. Tissue microarray, and immunohistochemistry with antibodies against Fra-1 was performed using the peroxidase and DAB methods. The target gene of miR-195 was determined by luciferase assay, quantitative RT-PCR and western blot. The regulation of motility by miR-195 was analyzed by western blot. RESULTS: miR-195 was frequently down-regulated in both prostate cancer cell lines, DU145 and PC3. Overexpression of miR-195 significantly repressed the capability of migration and invasion of prostate cancer cells. In addition, we identified Fra-1, a cell motility regulator, as a novel target of miR-195. Fra-1 was up-regulated in prostate cancer tissues. We also observed that inhibition of miR-195 or restoration of Fra-1 in miR-195-over-expressed prostate cancer cells partially reversed the suppressive effects of miR-195. Furthermore, we demonstrated miR-195 could inhibit prostate cancer cell motility by regulated the expression of c-Met, MMP1, MMP9. CONCLUSIONS: miR-195 can repress the migration and invasion of prostate cancer cells via regulating Fra-1. Our results indicate that miR-195 could be a tumor suppressor and may have a potential to be a diagnostics or therapeutic target in prostate cancer.

A meta-analysis including dose-response relationship between night shift work and the risk of colorectal cancer.

A meta-analysis was conducted to quantitatively evaluate the correlation between night shift work and the risk of colorectal cancer. We searched for publications up to March 2015 using PubMed, Web of Science, Cochrane Library, EMBASE and the Chinese National Knowledge Infrastructure databases, and the references of the retrieved articles and relevant reviews were also checked. OR and 95% CI were used to assess the degree of the correlation between night shift work and risk of colorectal cancer via fixed- or random-effect models. A dose-response meta-analysis was performed as well. The pooled OR estimates of the included studies illustrated that night shift work was correlated with an increased risk of colorectal cancer (OR = 1.318, 95% CI 1.121-1.551). No evidence of publication bias was detected. In the dose-response analysis, the rate of colorectal cancer increased by 11% for every 5 years increased in night shift work (OR = 1.11, 95% CI 1.03-1.20). In conclusion, this meta-analysis indicated that night shift work was associated with an increased risk of colorectal cancer. Further researches should be conducted to confirm our findings and clarify the potential biological mechanisms.