C1orf61 acts as a tumor activator in human hepatocellular carcinoma and is associated with tumorigenesis and metastasis

Hu, Haiming; Chen, Yi-Cheng; Liu, L.; Zhang, Chuan-Geng; Wang, Wei; Gong, Ke; Huang, Zan; Guo, Mingxiong; Li, Wenxin; Li, Wenhua

doi:10.1096/fj.12-216622

Cited by 17 publications

(19 citation statements)

References 57 publications

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Section: Resultsmentioning

confidence: 99%

“…One of these was C1orf61 ( Fig 2E ), which has been characterized as a tumor activator in hepatocellular carcinoma [48]. C1orf61 is located on 1q22, which experiences copy number amplifications in several cancers including hepatocellular carcinoma [48]. Investigation of the effect of upregulation of C1orf61 revealed that it was correlated with liver disease and HCC progression, and ectopic expression of C1ORF61 promoted cell proliferation, metastasis, and EMT [48].…”

Section: Resultsmentioning

confidence: 99%

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Epigenomic annotation of noncoding mutations identifies mutated pathways in primary liver cancer

Lowdon

Wang

2017

PLoS ONE

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Evidence that noncoding mutation can result in cancer driver events is mounting. However, it is more difficult to assign molecular biological consequences to noncoding mutations than to coding mutations, and a typical cancer genome contains many more noncoding mutations than protein-coding mutations. Accordingly, parsing functional noncoding mutation signal from noise remains an important challenge. Here we use an empirical approach to identify putatively functional noncoding somatic single nucleotide variants (SNVs) from liver cancer genomes. Annotation of candidate variants by publicly available epigenome datasets finds that 40.5% of SNVs fall in regulatory elements. When assigned to specific regulatory elements, we find that the distribution of regulatory element mutation mirrors that of nonsynonymous coding mutation, where few regulatory elements are recurrently mutated in a patient population but many are singly mutated. We find potential gain-of-binding site events among candidate SNVs, suggesting a mechanism of action for these variants. When aggregating noncoding somatic mutation in promoters, we find that genes in the ERBB signaling and MAPK signaling pathways are significantly enriched for promoter mutations. Altogether, our results suggest that functional somatic SNVs in cancer are sporadic, but occasionally occur in regulatory elements and may affect phenotype by creating binding sites for transcriptional regulators. Accordingly, we propose that noncoding mutation should be formally accounted for when determining gene- and pathway-mutation burden in cancer.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Epigenomic annotation of noncoding mutations identifies mutated pathways in primary liver cancer

Lowdon

Wang

2017

PLoS ONE

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“…The human breast tissue microarray chip was purchased from US Biomax Inc. (Rockville, MD, USA). Immunohistochemistry was performed as described by Hu et al 52 …”

Section: Methodsmentioning

confidence: 99%

“…The assay was performed as described by Hu et al 52 Images were acquired using a confocal microscope (Leica, Wetzlar, Germany).…”

Section: Methodsmentioning

confidence: 99%

Aberrant low expression of p85α in stromal fibroblasts promotes breast cancer cell metastasis through exosome-mediated paracrine Wnt10b

et al. 2017

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P85α, which acts as a tumour suppressor, is frequently found to be downregulated in various human cancers. However, the role of p85α in the tumour microenvironment is unknown. Here, we report that aberrantly low expression of p85α in breast cancer stroma is clinically relevant to breast cancer disease progression. Stromal fibroblasts can acquire the hallmarks of cancer-associated fibroblasts (CAFs) as a result of the loss of p85α expression. Paracrine Wnt10b from p85α-deficient fibroblasts can promote cancer progression via epithelial-to-mesenchymal transition (EMT) induced by the canonical Wnt pathway. Moreover, exosomes have a key role in paracrine Wnt10b transport from fibroblasts to breast cancer epithelial cells. Our results reveal that p85α expression in stromal fibroblasts haves a crucial role in regulating breast cancer tumourigenesis and progression by modifying stromal–epithelial crosstalk and remodelling the tumour microenvironment. Therefore, p85α can function as a tumour suppressor and represent a new candidate for diagnosis, prognosis and targeted therapy.

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“…As indicated above, the iTRAQ data suggest that Plac9 affect cell migration. To test this experimentally, two cell motility assays (wound-healing and cell invasion) were utilized as previously described [27]. As shown in Figure 8A&B, the wound-healing assay showed that wound closure for 16HBE-GFP-Plac9 was much faster than control group after 48h, indicating that Plac9 overexpression strongly enhanced cell migration.…”

Section: Effect Of Plac9 On Cellular Processes Including Cell Prolifementioning

confidence: 99%

Proteomic analysis reveals that Placenta-specific 9 induces cell proliferation and motility programs in human bronchial epithelial cells

Wang

Qin

Shen

et al. 2020

Preprint

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Abstract Background: Abnormal reprogramming of airway epithelium is a key cause of pulmonary diseases. The molecular mechanism underlying the abnormal reprogramming of airway epithelial cells (AECs) remains to be elucidated. Placenta-specific protein 9 (Plac9), a putative secretory protein, initially identified in placenta, has previously been shown to affect cell proliferation and motility in human embryonic hepatic cells. Results: Interestingly, we found that Plac9 was repressed in lung cancers (LCs) compared to the corresponding normal tissues. We further investigated the role of Plac9 in human bronchial epithelial cells by constructing a stable Plac9-overexpressing cell line (16HBE-GFP-Plac9) and analyzing the effect of Plac9 on cellular protein composition by using an isobaric tag for relative and absolute quantification (iTRAQ) proteomic approach. By gene ontology (GO) and pathway analyses, we found that GO terms and pathways associated with cell proliferation, cell cycle progression, and cell motility/migration were significantly enriched among the proteins regulated by Plac9. Consistently, we observed that overexpression of Plac9 reduced cell proliferation and altered cell cycle progression. In addition, it also increased cell motility, including migration and invasion. Conclusions: Our findings suggest that Plac9 inhibits cell proliferation through S phase arrest by altering cyclins/cyclin-dependent kinases (CDKs) and promotes cell motility likely via the concerted actions of cyclins, E-cadherin and vimentin, which may underlie Plac9-mediated abnormal human bronchial pathogenesis.

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C1orf61 acts as a tumor activator in human hepatocellular carcinoma and is associated with tumorigenesis and metastasis

Cited by 17 publications

References 57 publications

Epigenomic annotation of noncoding mutations identifies mutated pathways in primary liver cancer

Epigenomic annotation of noncoding mutations identifies mutated pathways in primary liver cancer

Aberrant low expression of p85α in stromal fibroblasts promotes breast cancer cell metastasis through exosome-mediated paracrine Wnt10b

Proteomic analysis reveals that Placenta-specific 9 induces cell proliferation and motility programs in human bronchial epithelial cells

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