Transcriptome analysis in primary colorectal cancer tissues from patients with and without liver metastases using next‐generation sequencing

Wang, Sen; Zhang, Chuan; Zhang, Zhiyuan; Qian, Wenwei; Sun, Ye; Ji, Bing; Zhang, Yue; Zhu, Chunyan; Ji, Dongjian; Wang, Qingyuan; Sun, Yueming

doi:10.1002/cam4.1147

Cited by 27 publications

(21 citation statements)

References 41 publications

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“…CCL27/CTACK has also been found to have higher expression in tumors than paratumorous colorectal tissues 30 . While CXCL6/GCPS expression was not altered in CRC tumors overall 31 , expression was lower in primary tumors of patients with disseminated CRC than in tumors that had not metastasized 32 .…”

Section: Discussionmentioning

confidence: 81%

Circulating inflammatory markers and colorectal cancer risk: A prospective case‐cohort study in Japan

Song

Sasazuki²,

Camargo

et al. 2018

Intl Journal of Cancer

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Blood levels of inflammation-related markers may reveal molecular pathways contributing to carcinogenesis. To date, prospective associations with colorectal cancer (CRC) risk have been based on few studies with limited sets of analytes. We conducted a case-cohort study within the Japan Public Health Center-based Prospective Study Cohort II, comparing 457 incident CRC cases during median 18 years follow-up with a random subcohort of 774 individuals. Baseline plasma levels of 62 cytokines, soluble receptors, acute-phase proteins, and growth factor markers were measured using Luminex bead-based assays. We estimated hazard ratios (HRs) associating each marker with CRC risk by Cox proportional hazards models adjusted for potential confounders. Subanalyses compared cases by years after blood draw (<5 vs. ≥5) and anatomical subsite (colon vs. rectum). Linear trends in quantiles of four C-C motif ligand (CCL) chemokines, one C-X-C motif ligand (CXCL) chemokine, and a soluble receptor were nominally associated with CRC risk based on p < 0.05, but none met false discovery rate corrected statistical significance. HRs for the 4th vs. 1st quartile were: 1.69 for CCL2/MCP1, 1.61 for soluble tumor necrosis factor receptor 2, 1.39 for CCL15/MIP1D, 1.35 for CCL27/CTACK, 0.70 for CXCL6/GCP2 and 0.61 for CCL3/MIP1A. Among cases diagnosed 5+ years after enrollment, CCL2/MCP1, CCL3/MIP1A and CXCL6/GCP2 retained nominal statistical significance. There were no significant differences in associations between colon and rectum. Our findings implicate chemokine alterations in colorectal carcinogenesis, but require replication for confirmation. Noninvasive chemokine assays may have potential application in colorectal cancer screening and etiologic research.

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Section: Discussionmentioning

confidence: 81%

Circulating inflammatory markers and colorectal cancer risk: A prospective case‐cohort study in Japan

Song

Sasazuki²,

Camargo

et al. 2018

Intl Journal of Cancer

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“…However, there were still several limitations in our study. Firstly, the sample number of normal tissues was not very large although previous studies with a small sample size also exist ( 36 ). Secondly the follow-up information of our patients was not enough to study the overall survival, most follow-up information after surgery was ~2–3 years.…”

Section: Discussionmentioning

confidence: 99%

Construction of a ceRNA network reveals potential lncRNA biomarkers in rectal adenocarcinoma

Zhang

Wang

et al. 2018

Oncol Rep

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Competing endogenous RNAs (ceRNAs) render the functions of long non-coding RNAs (lncRNAs) more complicated during cancer processes. Potential lncRNA biomarkers and their roles as ceRNAs have not been clearly described for rectal adenocarcinoma (READ). In the present study, we extracted data from The Cancer Genome Atlas (TCGA) including data from 167 tumor samples and 10 adjacent non-tumor samples. A total of 202 lncRNAs, 190 microRNAs (miRNAs) and 1,530 mRNAs were identified as READ-specific RNAs [log2(fold-change)>2, FDR<0.01]. The Gene Ontology (GO) biological processes and the Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathways were analysed for 1,530 specific mRNAs. Among 202 READ-specific lncRNAs, 7 lncRNAs were identified as being associated with overall survival of READ patients. Then, a ceRNA network was constructed with 34 key lncRNAs, 25 miRNAs and 65 mRNAs. A total of 7 lncRNAs from the network were revealed to be linked to clinical features. The results of qRT-PCR ascertained that our analysis was credible. Overall, this research provides a novel perspective from which to study the lncRNA-related ceRNA network in READ and assists in the identification of new potential biomarkers to be used for diagnostic and prognostic purposes.

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“…Immunohistochemistry was performed as previously described ( 17 ). The primary antibody used was GPR56 (diluted 1:200; cat.…”

Section: Methodsmentioning

confidence: 99%

GPR56 promotes proliferation of colorectal cancer cells and enhances metastasis via epithelial‑mesenchymal transition through PI3K/AKT signaling activation

Feng

Sun

et al. 2018

Oncol Rep

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G protein-coupled receptor 56 (GPR56), a member of the orphan GPCR family, has been reported to be an oncogene in various malignancies. However, little is known regarding the detailed molecular mechanism of GPR56 in colorectal cancer (CRC). The present study aimed to detect the expression level and biological function of GPR56 in CRC. We examined the expression of GPR56 in CRC tissues and cell lines by quantitative real time (qRT)-PCR, immunohistochemistry, and western blot analysis. The prognostic significance of GPR56 in CRC patients was evaluated by Kaplan-Meier survival analysis. The influence of GPR56 on tumor cell proliferation (via Cell Counting Kit-8, and a tumor formation assay in mice), apoptosis (flow cytometry), cell cycle distribution (flow cytometry) and migration (Transwell assay) was explored. We also investigated the underlying mechanism of GPR56 by western blot analysis. We found GPR56 expression was significantly upregulated in CRC tissues and cell lines compared to corresponding normal controls. Higher GPR56 expression in patients predicted poorer prognosis. Depletion of GPR56 markedly suppressed cell proliferation, migration, and invasion. GPR56 overexpression promoted CRC cell metastasis by expediting epithelial-mesenchymal transition by activating PI3K/AKT signaling. In conclusion, GPR56 played an important role in CRC progression and may represent a new therapeutic target to reduce CRC metastasis.

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Transcriptome analysis in primary colorectal cancer tissues from patients with and without liver metastases using next‐generation sequencing

Cited by 27 publications

References 41 publications

Circulating inflammatory markers and colorectal cancer risk: A prospective case‐cohort study in Japan

Circulating inflammatory markers and colorectal cancer risk: A prospective case‐cohort study in Japan

Construction of a ceRNA network reveals potential lncRNA biomarkers in rectal adenocarcinoma

GPR56 promotes proliferation of colorectal cancer cells and enhances metastasis via epithelial‑mesenchymal transition through PI3K/AKT signaling activation

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