ArticleMedical oncology (Northwood, London, England)2014
The role of c2orf68 and PI3K/Akt/mTOR pathway in human colorectal cancer.
Article in Medical oncology (Northwood, London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- C2ORF68 stabilizes SIVA1 to upregulate BCL-2 and suppress apoptosis in gallbladder cancer.Cell death discovery · 2026Article
- The Mechanistic Crosstalk between Probiotics, ncRNAs, and Autophagy: Implications for Colorectal Cancer Precision Medicine.Expert reviews in molecular medicine · 2026Review
- Mechanisms involved in the anti-tumor effects of Toosendanin in glioma cells.Cancer cell international · 2021Article
- Flavonoid GL-V9 suppresses invasion and migration of human colorectal cancer cells by inhibiting PI3K/Akt and MMP-2/9 signaling.Journal of Cancer · 2021Article
- Article
- Association between SET expression and glioblastoma cell apoptosis and proliferation.Oncology letters · 2016Article
- ClC-3 chloride channel modulates the proliferation and migration of osteosarcoma cells via AKT/GSK3β signaling pathway.International journal of clinical and experimental pathology · 2015Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the research is to determine whether c2orf68 gene plays a role in the carcinogenesis of human colorectal cancer and to study the function of c2orf68 belonging to the UPF0561 family. The mRNA expression levels of c2orf68 were examined in 30 pairs of human colorectal adenocarcinoma tissues and adjacent normal colorectal tissues by qRT-PCR. The SW480 and SW620 cell lines were transfected with siRNA against the c2orf68 gene and set gene. The expressed mRNA levels of Akt, PI3K, Bax, Bcl-2, caspase3, c-Myc, cyclinD1, pp2a and set were determined by qRT-PCR, and the protein levels of C2ORF68, c-Myc, PP2A and SET were examined by Western blot. Cell proliferation was tested by MTT assay, and apoptosis and cell cycle were studied by flow cytometry. Cancer metastasis assay was performed by transwell chamber. The c2orf68 mRNA expression was down-regulated in 63.33 % of the cancer samples, and a positive correlation was found between the mRNA expression of c-Myc and pp2a that of c2orf68. Meanwhile, there was a negative correlation between the mRNA expression of c2orf68 and set. The c2orf68 mRNA was significantly down-regulated in SW480(-c2orf68) and SW620(-c2orf68) cells. The inhibitory rate in the two cell lines was, respectively, 65.2 and 71.6 % by qRT-PCR. A 22.7 % inhibition on cell proliferation in SW480(-c2orf68) cells and a 21.2 % inhibition in SW620(-c2orf68) cells were observed using the MTT assay. Flow cytometry analysis indicates that the cell apoptosis rate was 21.42 % in SW480(-c2orf68) cells and 17.78 % in SW620(-c2orf68) cells, whereas the percentage of G1 phase cells was 61.8 and 58.6 % in SW480(-c2orf68) and SW620(-c2orf68) cells, respectively. In addition, the mRNA expression of set and Bax was up-regulated after c2orf68 interfered in SW480(-c2orf68) and SW620(-c2orf68) cells, whereas that of Bcl-2, c-Myc, cyclinD1, caspase3 and pp2a was down-regulated. Consistent with the mRNA results, the protein expression of C2ORF68, PP2A and c-Myc was down-regulated, whereas that of SET was up-regulated. Our data thus suggest that c2orf68 promotes carcinogenesis through the regulation of mammalian target of rapamycin signaling pathway.
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