ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
C6orf106 enhances NSCLC cell invasion by upregulating vimentin, and downregulating E-cadherin and P120ctn.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- ILRUN Promotes Atherosclerosis Through Lipid-Dependent and Lipid-Independent Factors.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Molecular characterisation of ILRUN, a novel inhibitor of proinflammatory and antimicrobial cytokines.Heliyon · 2020Article
- C6orf106 accelerates pancreatic cancer cell invasion and proliferation via activating ERK signaling pathway.Molecular and cellular biochemistry · 2019Article
- C6orf106 is a novel inhibitor of the interferon-regulatory factor 3-dependent innate antiviral response.The Journal of biological chemistry · 2018Article
- Ubiquitin-Binding Protein CG5445 Suppresses Aggregation and Cytotoxicity of Amyotrophic Lateral Sclerosis-Linked TDP-43 in Drosophila.Molecular and cellular biology · 2018Article
- TMEM17 depresses invasion and metastasis in lung cancer cells via ERK signaling pathway.Oncotarget · 2017Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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Abstract
Chromosome 6 open reading frame 106 (C6orf106) is a newly discovered protein; its expression and clinical pathological significance in human tumors remains unclear. Immunohistochemistry, Western blot, and immunofluorescence were performed to assess C6orf106 expression in non-small cell lung cancer (NSCLC). In addition, the relationships between subcellular localization and clinical pathological factors were analyzed. Through C6orf106 overexpression and repression, respectively, in lung cancer cell lines, we explored the effect of this molecule on NSCLC invasion abilities. C6orf106 was highly expressed in the cytoplasm of lung cancer tissue cells (60.4 %, 75/124), compared with adjacent normal lung tissues (15.2 %, 7/46, p < 0.001). In addition, its expression was positively correlated with differentiation (p = 0.001), TNM stage (p = 0.011), lymph node metastasis (p = 0.018), and poor prognosis (p = 0.006). Furthermore, C6orf106 overexpression enhanced NSCLC cell invasion. Moreover, C6orf106 was shown to increase vimentin expression, while decreasing E-cadherin and P120ctn. C6orf106 is highly expressed in NSCLC and correlates with clinical and pathological factors, as well as poor prognosis. C6orf106 promotes invasion in NSCLC cells. Finally, C6orf106 upregulates vimentin, and downregulates E-cadherin and P120ctn.
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