Colorectal cancer: Metastases to a single organ

Vatandoust, Sina; Price, Timothy; Karapetis, Christos S.

doi:10.3748/wjg.v21.i41.11767

Cited by 260 publications

(223 citation statements)

References 139 publications

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“…Vatandoust et al reported that patients with PM CRC who underwent curative surgery could expect long-term survival (28). Similarly to Vatandoust et al's report, MSI-H-PM also conferred a better prognosis in patients with curatively resected stage IV CRC in our study.…”

Section: Survival Analysis Of Patients With Stage IV Colorectal Cansupporting

confidence: 87%

Metastatic Pattern of Stage IV Colorectal Cancer with High-Frequency Microsatellite Instability as a Prognostic Factor

Fujiyoshi

Yamamoto

Takenoya

et al. 2017

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Abstract. Background: A recent clinical trial on the immune check-point inhibitor pembrolizumab demonstrated that microsatellite instability (MSI) is a good biomarker for response to this inhibitor. However, clinicopathological features of advanced colorectal cancer (CRC) with high-frequency MSI (MSI-H) are unclear. Patients and MethodsColorectal cancer (CRC) is the third most commonly diagnosed cancer and frequent cause of cancer-related death worldwide (1). Specifically, the 5-year survival rate of patients with advanced CRC is less than 30%, and further advances in chemotherapy and surgical techniques are required to improve the survival rate of patients with CRC. Recently, novel molecular-targeting drugs, such as antibody to epidermal growth factor receptor (EGFR), are based on the molecular mechanism of carcinogenesis and achieve good efficacy. However, biomarkers are often required for appropriate therapy and are predicted based on the molecular mechanism of carcinogenesis.During carcinogenesis, genetic changes, including deletion, insertion and substitution of nucleotides, rearrangement and epigenetic changes are accumulated. At least two types of genetic changes are known: chromosomal instability (CIN) and microsatellite instability (MSI). CIN comprises of structural and numerical changes of chromosomes, whereas MSI comprises frequent mutations in the microsatellite area without obvious structural and numerical changes of chromosomes. It has been reported that in Western countries approximately 80% of CRCs exhibit CIN and 15% have MSI (2). MSI is caused by dysfunction of the mismatch repair system, which detects and repairs mismatches that occur during DNA replication (3, 4). CRCs with CIN and MSI demonstrate different clinicopathological features, probably because of different mechanisms of genetic changes (5).Sporadic CRC with high-frequency MSI (MSI-H) is prone to develop in the proximal colon and in older females. Pathological characteristics are associated with the presence of tumour-infiltrating lymphocytes, a Crohn's-like lymphocytic reaction and mucinous/signet ring cell differentiation (6-9). Although CRC with MSI-H is indicative of good prognosis in stage II and III disease (10-12), several reports suggest that the prognosis of CRC with MSI-H is poorer than that of 239 Τhis article is freely accessible online.

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Section: Survival Analysis Of Patients With Stage IV Colorectal Cansupporting

confidence: 87%

Metastatic Pattern of Stage IV Colorectal Cancer with High-Frequency Microsatellite Instability as a Prognostic Factor

Fujiyoshi

Yamamoto

Takenoya

et al. 2017

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“…Cancer invasion and distant metastasis, which are complex, multistep processes that are likely controlled by various genetic and/or epigenetic changes, are the leading causes of more than 90% of cancer-related deaths, including CRC deaths [22]. However, the regulatory factors that are responsible for molecular changes that initiate metastatic progression have not been defined.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-375 suppresses human colorectal cancer metastasis by targeting Frizzled 8

Wen

Liu

et al. 2016

Oncotarget

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microRNAs are aberrantly expressed during the development and progression of a variety of human cancers, including colorectal cancer (CRC). Of these microRNAs, microRNA-375 (miR-375) was previously observed to be downregulated in human colorectal cancer(CRC) plasma and tissues, but its functions are largely unknown. Here, we investigated the impact of miR-375 on CRC metastasis. Specifically, miR-375 expression was significantly decreased in human CRC tissues compared with their matched noncancerous tissues (NCTs), and low levels of miR-375 predicted tumor metastatic potential. The up-regulation of miR-375 suppressed colorectal cancer cell migration and invasion in vitro and reduced tumor metastases in murine models established by both orthotopic implantation and spleen injection. Furthermore, we identified Frizzled 8 (FZD8) as a direct target of miR-375 in CRC, and miR-375 negatively regulated Wnt/β-catenin signaling by suppressing FZD8. More importantly, FZD8 expression inversely correlated with overall survival in human CRC patients and is a likely independent predictor of survival. Therefore, we concluded that miR-375 functions as a tumor-suppressive microRNA by directly acting upon FZD8, which may serve as a new therapeutic target to inhibit tumor metastasis in CRC.

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“…Metastasis is the dominant cause of death in patients with colon cancer [3]. The mechanisms behind colon cancer metastasis remains elusive but accumulating data indicate that increased expression of adhesion molecules and chemokines facilitate colon cancer migration and spread [4].…”

Section: Introductionmentioning

confidence: 99%

MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA

2017

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Colorectal cancer is the second most common cause of cancer-related death, which is due to migration of tumor cells to distant sites of metastasis. Accumulating data indicate that mciroRNAs play an important role in several aspects of colon cancer cell biology. Herein, we examined the role of miR-155-5p in colon cancer cell migration induced by the CCL17-CCR4 axis in HT-29 colon cancer cells. We found that miR-155-5p knockdown in serum starved colon cancer cells decreased CCL17-induced cell chemotaxis. Moreover, knocking down miR-155-5p markedly decreased CCL17-provoked activation of RhoA in colon cancer cells. Bioinformatics analysis predicted two putative binding sites in the AU-rich element at the 3′-UTR of RhoA mRNA. MiR-155-5p binding to RhoA mRNA was verified using a target site blocker and functionally validated by RNA immunoprecipitation assays, showing that miR-155-5p-dependent regulation of RhoA mRNA is mediated by AU-rich elements present in the 3′-UTR region. Taken together, these results show that miR-155-5p positively regulates RhoA mRNA levels and translation as well as cell migration in serum starved colon cancer cells and indicate that targeting miR-155-5p might be a useful strategy to antagonize colon cancer metastasis.

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Colorectal cancer: Metastases to a single organ

Cited by 260 publications

References 139 publications

Metastatic Pattern of Stage IV Colorectal Cancer with High-Frequency Microsatellite Instability as a Prognostic Factor

Metastatic Pattern of Stage IV Colorectal Cancer with High-Frequency Microsatellite Instability as a Prognostic Factor

MicroRNA-375 suppresses human colorectal cancer metastasis by targeting Frizzled 8

MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA

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