ArticleThe American journal of pathology2006
H-REV107-1 stimulates growth in non-small cell lung carcinomas via the activation of mitogenic signaling.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- PLA2G16 expression predicts prognosis and gemcitabine sensitivity in patients with pancreatic cancer.PeerJ · 2025Article
- Targeting PLA2G16, a lipid metabolism gene, by Ginsenoside Compound K to suppress the malignant progression of colorectal cancer.Journal of advanced research · 2022Article
- A novel lncRNA ROPM-mediated lipid metabolism governs breast cancer stem cell properties.Journal of hematology & oncology · 2021Article
- Protein Dynamics Influence the Enzymatic Activity of Phospholipase A/Acyltransferases 3 and 4.Biochemistry · 2021Article
- Relationship between polymorphisms of the lipid metabolism-related gene PLA2G16 and risk of colorectal cancer in the Chinese population.Functional & integrative genomics · 2019Article
- Screening of urine identifies PLA2G16 as a field defect methylation biomarker for prostate cancer detection.PloS one · 2019Article
- miR-142-5p suppresses proliferation and promotes apoptosis of human osteosarcoma cell line, HOS, by targeting PLA2G16 through the ERK1/2 signaling pathway.Oncology letters · 2019Article
- Diagnostic investigations of PLA2G16 and CDH11 expression levels as independent prognostic markers of human osteosarcoma.Archives of medical science : AMS · 2017Article
- High expression of PLA2G16 is associated with a better prognosis in HER2-positive breast cancer.Journal of thoracic disease · 2017Article
- Article
- The HRASLS (PLA/AT) subfamily of enzymes.Journal of biomedical science · 2015Review
- PLA2G16 Expression in Human Osteosarcoma Is Associated with Pulmonary Metastasis and Poor Prognosis.PloS one · 2015Article
- Pla2g16 phospholipase mediates gain-of-function activities of mutant p53.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Phospholipase A/Acyltransferase enzyme activity of H-rev107 inhibits the H-RAS signaling pathway.Journal of biomedical science · 2014Article
- H-rev107 regulates prostaglandin D2 synthase-mediated suppression of cellular invasion in testicular cancer cells.Journal of biomedical science · 2013Article
- Induction of apoptosis by the retinoid inducible growth regulator RIG1 depends on the NC motif in HtTA cervical cancer cells.BMC cell biology · 2009Article
- Identification and functional characterization of adipose-specific phospholipase A2 (AdPLA).The Journal of biological chemistry · 2008Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
H-REV107-1, a known member of the class II tumor suppressor gene family, is involved in the regulation of differentiation and survival. We analyzed H-REV107-1 in non-small cell lung carcinomas, in normal lung, and in immortalized and tumor-derived cell lines. Sixty-eight percent of lung tumors revealed positive H-REV107-1-specific staining. Furthermore, survival analysis demonstrated a significant association of cytoplasmic H-REV107-1 with decreased patient survival. This suggested that H-REV107-1, known as a tumor suppressor, plays a different role in non-small cell lung carcinomas. Knock-down of H-REV107-1 expression in lung carcinoma cells inhibited anchorage-dependent and anchorage-independent growth whereas overexpression of H-REV107-1 induced tumor cell proliferation. Consistent with results of the survival analysis, cytoplasmic localization of the protein was essential for this growth-inducing function. Analysis of signaling pathways potentially involved in this process demonstrated that overexpression of H-REV107-1 stimulated RAS-GTPase activity, ERK1,2 phosphorylation, and caveolin-1 expression in the cell lines analyzed. These results indicate that H-REV107-1 is deficient in its function as a tumor suppressor in non-small cell lung carcinomas and is required for proliferation and anchorage-independent growth in cells expressing high levels of the protein, thus contributing to tumor progression in a subset of non-small cell lung carcinomas.
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