Ulcerative colitis-associated colorectal cancer

Yashiro, Masakazu

doi:10.3748/wjg.v20.i44.16389

Cited by 212 publications

(176 citation statements)

References 105 publications

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“…Interestingly, upregulated expression of IL-1β, IL-6, and TNF-α, and sustained activation of the STAT1, STAT3, and JNK pathways, both occur in LCN2-knockout mice along with an increase in the susceptibility to infection with Klebsiella pneumoniae or Escherichia coli in the liver and in mice with breast cancer [33, 34]. It has been noted that inflammation of the colon, including inflammatory bowel disease (IBD) or colitis, increases the risk of CRC by causing a cellular immune response and accumulating genetic alterations that might trigger specific oncogenic pathways [35, 36]. Besides, the finding that the long-term prognosis of CRC is poorer in patients with IBD than in those with sporadic CRC [37] implies that elevated LCN2 expression plays a prominent role in CRC progression.…”

Section: Discussionmentioning

confidence: 99%

Lipocalin2 suppresses metastasis of colorectal cancer by attenuating NF-κB-dependent activation of snail and epithelial mesenchymal transition

Feng

Chen

et al. 2016

Mol Cancer

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BackgroundLipocalin2 (LCN2) is a secretory protein that is aberrantly expressed in several types of cancer and has been involved in metastatic progression. However, neither mechanisms nor the role that LCN2 plays in the metastasis of colorectal cancer are clear.MethodsLCN2 expression in colorectal cancer was detected by immunohistochemistry in 400 tissue specimens and Kaplan-Meier survival analysis was performed. In vitro, real-time PCR, western blot, colony formation assay, immunofluorescence assay, wound healing assay, migration and invasion experiment were performed to investigate the effects of LCN2 in epithelial mesenchymal transition (EMT), migration and invasion, respectively. In vivo mouse xenograft and metastasis models were utilized to determine tumorigenicity and metastasis ability, and immunohistochemistry, real-time PCR, western blot were used to evaluate the related protein expression. Luciferase reporter assay was used to explore the role of LCN2 on NF-ĸB promoter.ResultsLCN2 was highly expressed in 66.5% of the specimens, and significantly correlated with positive E-cadherin in the membrane and negative nuclear β-catenin. Higher expression of LCN2 together with negative NF-κB expression was negatively related to nuclear accumulation of snail and predicted favorable prognosis. LCN2 blocked cell proliferation, migration and invasion in vitro and in vivo, and inhibited translocation of NF-κB into nucleus. NF-κB could reverse the effect of LCN2 on EMT and promote snail expression. Rescued snail expression had similar effect without influencing NF-κB activity.ConclusionLCN2 may be an important negative regulator in EMT, invasion and metastasis of CRC via acting as upstream of NF-κB/snail signaling pathway. Thereby combinative manipulation of LCN2 and NF-κB/snail pathway may represent a novel and promising therapeutic approach for the patients with CRC.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-016-0564-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Lipocalin2 suppresses metastasis of colorectal cancer by attenuating NF-κB-dependent activation of snail and epithelial mesenchymal transition

Feng

Chen

et al. 2016

Mol Cancer

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“…According to Crohn’s and Colitis Foundation of America (CCFA) report, about 1.6 million Americans are aﬄicted with IBD. Furthermore, IBD is commonly recognized as one of the leading causative risk factors for the progression of colorectal cancer mediated through chronic intestinal inflammation [6, 7]. Despite significant advances in patient care, clinical data showed low remission rates at best of 40%.…”

Section: Introductionmentioning

confidence: 99%

Disruption of GPR35 Exacerbates Dextran Sulfate Sodium-Induced Colitis in Mice

Farooq

Hou

et al. 2018

Dig Dis Sci

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“…In contrast to UC, the role of CD in CRC risk remains controversial, and the majority of studies could not detect different incidence rates in comparison with the general population (8). Relative to sporadic CRC, CAC is usually linked to an earlier age of onset, a fast progressing course and a higher rate of mortality (9). Approximately 59% of CAC patients were deceased at the 5-year follow-up according to the statistics of Ording et al (10).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑449a is a potential predictor of colitis‑associated colorectal cancer progression

Feng

Song

et al. 2018

Oncol Rep

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An early diagnosis of colitis‑associated colorectal cancer (CAC) is important for its clinical management. However, it is currently difficult to distinguish the different stages of CAC development. MicroRNA dysregulation is common in human colorectal disorders, however little is known regarding whether miRNA affects tumor progression by regulating inflammation. In the present study, we identified a novel miRNA (miR‑449a), the expression of which was significantly reduced in CAC tissues than in paired adjacent non‑cancerous tissues (ANTs). Notably, the level of miR‑449a was in a markedly decreased pattern during the neoplastic transformation of ulcerative colitis (UC)‑to‑CAC, as demonstrated by both clinical investigations and the experimental mouse model induced by AOM/DSS treatment. In addition, we observed that decreased miR‑449a expression was associated with advanced T or N status, later clinical stage and poor histological differentiation of CAC. Mechanistic studies revealed that miR‑449a inhibited the growth and metastasis of human colon cancer cells by directly binding to the 3'‑UTR of Notch‑1 and thereby, suppressed the activation of the Notch signaling pathway. Therefore, these findings provide strong evidence for the translational potential of miR‑449a in the discrimination of patients with UC that is likely to progress into CAC, from those unlikely to progress, as well as in the prognosis and diagnosis of CAC.

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Ulcerative colitis-associated colorectal cancer

Cited by 212 publications

References 105 publications

Lipocalin2 suppresses metastasis of colorectal cancer by attenuating NF-κB-dependent activation of snail and epithelial mesenchymal transition

Lipocalin2 suppresses metastasis of colorectal cancer by attenuating NF-κB-dependent activation of snail and epithelial mesenchymal transition

Disruption of GPR35 Exacerbates Dextran Sulfate Sodium-Induced Colitis in Mice

MicroRNA‑449a is a potential predictor of colitis‑associated colorectal cancer progression

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