ArticleMedical oncology (Northwood, London, England)2016
hcrcn81 promotes cell proliferation through Wnt signaling pathway in colorectal cancer.
Article in Medical oncology (Northwood, London, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Paeonol exerts anti‑tumor activity against colorectal cancer cells by inducing G0/G1 phase arrest and cell apoptosis via inhibiting the Wnt/β‑catenin signaling pathway.International journal of molecular medicine · 2020Article
- Colony stimulating factor-1 receptor promotes proliferation, migration and invasion in the human nasopharyngeal carcinoma 6-10B cell line via the phosphoinositide 3-kinase/Akt pathway.Oncology letters · 2018Article
- Differential expression profiles of long noncoding RNA and mRNA in colorectal cancer tissues from patients with lung metastasis.Molecular medicine reports · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The objective of the study was to investigate the role of hcrcn81 gene in Wnt/β-catenin signaling pathway related to human colorectal cancer. A total of 30 pairs of human colorectal cancer tissues with control normal tissues were analyzed by qRT-PCR. The proliferation, apoptosis, cell cycle, cell colony and metastasis of LS174T(-hcrcn81), HCT116(-hcrcn81), LoVo(+hcrcn81) and SMMC-7721(+hcrcn81) cells were tested, of which hcrcn81 was knockdown in LS174T, HCT116 cells and hcrcn81 was overexpressed in LoVo, SMMC-7721 cells. Besides, the mRNA and protein levels of hcrcn81, β-catenin, c-Myc, cyclinD1, GSK-3β and survivin in colon cancer cell lines were evaluated by qRT-PCR and western blot. The mRNA levels of β-catenin and Survivin were up-regulated in 76.7 % (23/30) and 63.3 % (19/30) of the tumor samples, respectively. hcrcn81 and GSK-3β mRNA expression levels were down-regulated in 20/30 (66.7 %) and 21/30 (70.0 %) of the tumor samples as compared to the adjacent normal tissues, respectively. Furthermore, in LoVo(+hcrcn81) and SMMC-7721(+hcrcn81) cells, the mRNA and protein levels of β-catenin, c-Myc, cyclinD1 and Survivin were up-regulated, whereas those of GSK-3 were down-regulated. In LS174T(-hcrcn81) and HCT116(-hcrcn81) cells, the mRNA levels of β-catenin, c-Myc, cyclinD1 and Survivin were down-regulated, whereas GSK-3βmRNA was up-regulated. Cell proliferation in LoVo(+hcrcn81) and SMMC-7721(+hcrcn81) groups was significantly enhanced (P < 0.05). Proliferation index in both LoVo(+hcrcn81) and SMMC-7721(+hcrcn81) groups was significantly higher than that in the control groups (P < 0.05). The number of colony in LoVo(+hcrcn81) and SMMC-7721(+hcrcn81) cells were significantly higher than that in the control groups (P < 0.05). In addition, the percentage of apoptotic cells in LoVo(+hcrcn81) and SMMC-7721(+hcrcn81) groups were significantly lower than that in the control groups (P < 0.01, P < 0.01). Finally, the number of migrating cells was significantly higher in LoVo(+hcrcn81) and SMMC-7721(+hcrcn81) groups than that in the control group (P < 0.05). hcrcn81 might promote carcinogenesis and progression through regulation of the Wnt/β-catenin signaling pathway and plays an important role in the carcinogenesis of colorectal cancer.
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