The prognostic value of lymphovascular invasion (LVI) in stage I/II colorectal cancer (CRC) does not reach a consensus. To systematically assess prognostic significance of LVI, databases of PubMed, Web of Science, and Embase were searched from inception up to 10 Dec 2016. The pooled hazard ratio (HR) and 95% confidence intervals (CI) were used to determine the prognostic effects. Nineteen relevant studies including 9881 total patients were enrolled. Our results showed that LVI is significantly associated with poor prognosis in overall survival (OS) (HR=2.15, 95 % CI=1.72–2.68, P < 0.01) and disease-free survival (DFS) (HR=1.73, 95% CI=1.50–1.99, P < 0.01), which is similar in stage II patients. Further subgroup analysis revealed that the significance of the association between LVI and worse prognosis in CRC patients is not affected by below factors, including geographic setting, LVI positive rate, treatment, tumor site, and quality of the study. The current meta-analysis suggests that LVI may be a poor prognostic factor for stage I/II CRC patients.

Colorectal cancer (CRC) is one of the most common types of malignancy worldwide. Distant metastasis is a key cause of CRC-associated mortality. MEIS2 has been identified to be dysregulated in several types of human cancer. However, the mechanisms underlying the regulatory role of MEIS2 in CRC metastasis remain largely unknown. For the first time, the present study demonstrated that MEIS2 serves a role as a promoter of metastasis in CRC. In vivo and in vitro experiments revealed that knockdown of MEIS2 significantly suppressed CRC migration, invasion and the epithelial-mesenchymal transition. Furthermore, microarray and bioinformatics analyses were performed to investigate the underlying mechanisms of MEIS2 in the regulation of CRC metastasis. Additionally, it was identified that a high expression of MEIS2 was significantly associated with a shorter overall survival time for patients with CRC. The present study demonstrated that MEIS2 may serve as a novel biomarker for CRC.

Heat shock factor 1 (HSF1) is a powerful multifaceted oncogenic modifier that plays a role in maintaining the protein balance of cancer cells under various stresses. In recent studies, there have been reports of increased expression of HSF1 in colorectal cancer (CRC) cells, and the depletion of the HSF1 gene knockdown has inhibited colon cancer growth both in vivo and in vitro. Therefore, HSF1 is a promising target for colon cancer treatment and chemoprevention. In the present study, we found that Schizandrin A (Sch A) significantly inhibited the growth of CRC cell lines by inducing cell cycle arrest, apoptosis and death. Through HSE luciferase reporter assay and quantitative PCR (qPCR), we identified Sch A as a novel HSF1 inhibitor. In addition, Sch A could effectively inhibit the induction of HSF1 target proteins such as heat-shock protein (HSP) 70 (HSP70) and HSP27, whether in heat shock or normal temperature culture. In the Surface Plasmon Resonance (SPR) experiment, Sch A showed moderate affinity with HSF1, further confirming that Sch A might be a direct HSF1 inhibitor. The molecular docking and molecular dynamic simulation results of HSF1/Sch A suggested that Sch A formed key hydrogen bond and hydrophobic interactions with HSF1, which may contribute to its potent HSF1 inhibition. These findings provide clues for the design of novel HSF1 inhibitors and drug candidates for colon cancer treatment.

To provide a quantitative assessment of the association between iron intake, serum iron indices and the risk of colorectal adenoma (CRA), we summarised the evidence from observational studies. Relevant studies were identified in MEDLINE and EMBASE until 31 March 2015. Summary relative risks (SRRs) with 95% confidence intervals (CIs) were pooled with a random-effects model. A total of 10 articles, involving 3318 subjects with CRA, were used in this meta-analysis. The SRR of CRA was 0.83 (95% CI: 0.71-0.98; P = 0.694, I = 0) for the highest versus the lowest level of dietary iron intake. The SRR was 0.93 (95% CI: 0.62-1.42) for total (dietary and supplemental) iron intake, 1.23 (95% CI: 1.03-1.48) for haem iron intake and 0.73 (95% CI: 0.54-0.97) for supplemental iron intake. Serum iron indices were not associated with CRA risk (serum ferritin: SRR = 1.16, 95% CI: 0.81-1.66; serum iron: SRR = 1.02, 95% CI: 0.75-1.38; serum transferrin saturation: SRR = 1.01; 95% CI: 0.82-1.50). Increased intake of haem iron is associated with significantly increased risk of CRA, whereas intake of non-haem or supplemental iron is inversely associated with risk of CRA. Limited data indicate null associations between serum iron indices and CRA risk.

Background: Complete mesocolic excision (CME) emphasizes sharp dissection along the mesocolon plane and ligation of the supplying vessels at their origin. Although laparoscopic CME is reported to be feasible and safe, the benefit of laparoscopic CME over noncomplete mesocolic excision (NCME) remains unclear. This meta-analysis aimed to compare the safety, quality, and effect of laparoscopic CME with NCME. Materials and Methods:A systematic literature search with no limits was performed in PubMed, Embase, and Web of Science on March 27, 2020. Studies comparing laparoscopic CME with NCME were enrolled. Outcomes of interests included intraoperative, pathologic, postoperative, and survival outcomes.Results: Seven studies (5 articles and 2 conference abstracts) published between 2015 and 2020 with a total of 1595 patients (742 by CME and 853 by NCME) were enrolled. Compared with NCME, laparoscopic CME was associated with less intraoperative blood loss [P < 0.001, weighted mean difference (WMD) = −12.01, 95% confidence interval (CI): −13.56 to −10.45, I 2 = 44%], more harvested lymph nodes (P < 0.001, WMD = 6.50, 95% CI: 3.57-9.42, I 2 = 89%), longer length of specimens (P = 0.004, WMD = 3.57, 95% CI: 1.12-6.03, I 2 = 93%), longer distance from tumor to high tie (P < 0.001, WMD = 1.36, 95% CI: 0.87-1.85, I 2 = 76%), and longer distance from nearest bowel wall to high tie (P < 0.001, WMD = 1.36, 95% CI: 0.87-1.85, I 2 = 85%). No differences were observed in terms of operative time, postoperative complications, wound infection, ileus, proximal, and distal resection margin or disease-free survival between 2 groups. Conclusions:The currently limited evidences suggest that laparoscopic CME can slightly decrease intraoperative blood loss and improve specimen quality, but its safety and survival benefits need to be further studied. High-quality evidences are needed before laparoscopic CME can be recommended as the standard procedure for colon cancer surgery.

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In this paper, a facile aqueous route to water-soluble CdSe/CdS quantum dots (QDs) under mild conditions has been developed. The samples were characterized by means of transmission electron microscopy, energy-dispersive X-ray spectroscopy, and photoluminescence (PL) spectroscopy. The PL property of the QDs can be controlled by adjusting the reaction time. The CdSe/CdS QDs after 48-h reaction with size of 5 nm have the strongest PL intensity located at 553 nm, and the highest quantum yield of 19.9 %. The obtained QDs were applied for the colorectal cancer screening. The QDs could be conjugated with antibody of aldo-keto reductase family 1, member B10 (AKR1B10) for the detection of AKR1B10. The AKR1B10 in PBS/5 % serum solution with concentration of 1 ng/mL could be well calibrated, and the limit of detection could be lower than 0.05 ng/mL.Keywords CdSe/CdS quantum dots Á Water soluble Á Colorectal cancer Á Aldo-keto reductase family 1, member B10 (AKR1B10) Á Nanomedicine Á Health effects

Objective. BHLHE41 has been shown to be a marker of tumorigenesis. Colon cancer (CC) is a common malignant tumor of colonic mucosa. This study mainly explored the mechanism of BHLHE41 in alleviating malignant behavior of hypoxia-induced CC cells. Methods. The levels of BHLHE41 in CC and normal cell lines were tested by Western blot and qRT-PCR. After, CC cells were subjected to hypoxia treatment and BHLHE41 overexpression transfection, and the BHLHE41 expression, the effect of BHLHE41 on CC cell viability, apoptosis, migration, and invasion and cell cycle were tested by qRT-PCR and relevant cell functional experiments. HIF-1α and epithelial-mesenchymal transition- (EMT-) related proteins were tested by Western blot. Moreover, CC tumor-bearing model was established in nude mice, and the effect of BHLHE41 on the tumor was evaluated by measuring the tumor volume and weight. Then, the expressions of BHLHE41 and EMT-related proteins were detected by immunohistochemistry and Western blot. Results. Western blot and qRT-PCR showed that BHLHE41 was lowly expressed in CC cells. BHLHE41 overexpression could inhibit the hypoxia-induced CC cell viability, migration, and invasion, induce apoptosis, and alter cell cycle. Besides, BHLHE41 overexpression could enhance the levels of E-cadherin but reduce the levels of HIF-1α, N-cadherin, vimentin, and MMP9 in hypoxia-induced CC cells. Moreover, BHLHE41 overexpression reduced tumor volume, weight, and EMT-related proteins levels in tumor tissues. Conclusions. BHLHE41 overexpression could mitigate the malignant behavior of hypoxia-induced CC via modulating the HIF-1α/EMT pathway.