ArticleMolecular biology reports2019
Expression of long non-coding RNA CCHE1 in colorectal carcinoma: correlations with clinicopathological features and ERK/COX-2 pathway.
Article in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- A Diagnostic Panel for Acquired Immune-Mediated Polyneuropathies Based on the Expression of lncRNAs.Frontiers in immunology · 2021Trial
- Non-coding RNAs: modulators of signaling pathways and prognostic biomarkers in digestive system cancer.Molecular cancer · 2026Review
- Exploring the prognostic significance of iron death‑related lncRNAs in colorectal cancer: A systematic review and meta‑analysis.Oncology letters · 2024Article
- Decoding the regulatory landscape of lncRNAs as potential diagnostic and prognostic biomarkers for gastric and colorectal cancers.Clinical and experimental medicine · 2024Review
- Research Progress on the Pathogenesis of Knee Osteoarthritis.Orthopaedic surgery · 2023Review
- lncRNA-PACER upregulatesGastroenterology report · 2021Article
- Expression profiles of long non-coding RNAs in the cartilage of patients with knee osteoarthritis and normal individuals.Experimental and therapeutic medicine · 2021Article
- Upregulation of cervical carcinoma expressed PCNA regulatory long non-coding RNA promotes esophageal squamous cell carcinoma progression.Oncology letters · 2020Article
- The Role of Long Noncoding RNAs in Human Papillomavirus-associated Pathogenesis.Pathogens (Basel, Switzerland) · 2020Review
- Long non-coding RNA ROR1-AS1 induces tumorigenesis of colorectal cancer by affecting Wnt/β-catenin signaling pathway.Bioscience reports · 2019Article
- Knockdown of lncRNA CCEPR suppresses colorectal cancer progression.Experimental and therapeutic medicine · 2019Article
- LINC00052 suppressed glioma cell proliferation and invasion by downregulating insulin-like growth factor 2.Translational cancer research · 2019Article
- Cervical carcinoma high-expressed long non-coding RNA 1 may promote growth of colon adenocarcinoma through interleukin-17A.Oncology letters · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is among the leading causes of cancer-related mortality worldwide. Compelling evidence suggests that long non-coding RNA (lncRNAs) can control carcinogenesis by regulating various aspects of cell biology. However, limited number of CRC-related lncRNAs has been well characterized. This study was undertaken to investigate the expression pattern of the novel lncRNA-CCHE1 in CRC patients and to examine its correlation with clinicopathological features, ERK/COX-2 pathway and some cell proliferation markers in order to gain biological insights on its role in CRC pathogenesis. Colon cancer specimens with their adjacent non-cancerous tissues were taken from 60 patients with primary CRC. LncRNA-CCHE1 relative expression was assessed using quantitative real-time RT-PCR. P-ERK ½ and cyclin D1 levels were estimated by ELISA. COX-2 and proliferating cell nuclear antigen (PCNA) expression were assessed immunohistochemically. lncRNA-CCHE1 expression was upregulated in CRC tissues compared to adjacent non-cancerous tissues, and was significantly associated with larger tumor size, less differentiated histology, advanced dukes' stage, positive lymph node involvement and vascular invasion. It also showed a significant positive correlation with the expression of p-ERK1/2, COX-2 as well as cyclin D1and PCNA (as markers for cell proliferation). These findings signify that lncRNA-CCHE1 is a key oncogene possibly involved in CRC development and progression by modulating ERK/COX-2 pathway and cell proliferation activity. Our study also provides a rationale for potential use of lncRNA-CCHE1 as a novel prognostic marker, and opens the door for the development of lncRNA-CCHE1-directed therapeutic approaches for CRC patients.
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