ArticleNature communications2016
Genome-wide RNAi screening identifies TMIGD3 isoform1 as a suppressor of NF-κB and osteosarcoma progression.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
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- Comprehensive Investigation Illustrates the Role of M2 Macrophages and Its Related Genes in Pancreatic Cancer.Medicina (Kaunas, Lithuania) · 2023Article
- Prediction and Identification of GPCRs Targeting for Drug Repurposing in Osteosarcoma.Frontiers in oncology · 2022Article
- Identification of Gαi3 as a promising target for osteosarcoma treatment.International journal of biological sciences · 2022Article
- The NF-κB pathway is critically implicated in the oncogenic phenotype of human osteosarcoma cells.Journal of applied biomedicine · 2021Article
- Adenosine A3 receptor activated in HAnnals of translational medicine · 2021Article
- Microenvironment-related prognostic genes in esophageal cancer.Translational cancer research · 2020Article
- Theabrownin inhibits the cytoskeleton‑dependent cell cycle, migration and invasion of human osteosarcoma cells through NF‑κB pathway‑related mechanisms.Oncology reports · 2020Article
- Characterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma.Aging · 2020Article
- Identification of biomarkers for the diagnosis and treatment of primary colorectal cancer based on microarray technology.Translational cancer research · 2020Article
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- The role of GPCRs in bone diseases and dysfunctions.Bone research · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The ability of cancer cells to survive and grow in anchorage- and serum-independent conditions is well correlated with their aggressiveness. Here, using a human whole-genome shRNA library, we identify TMIGD3 isoform1 (i1) as a factor that suppresses this ability in osteosarcoma (OS) cells, mainly by inhibiting NF-κB activity. Knockdown of TMIGD3 increases proliferation, tumour formation and metastasis of OS cells. Overexpression of TMIGD3 isoform1 (i1), but not isoform3 (i3) which shares a common C-terminal region, suppresses these malignant properties. Adenosine A3 receptor (A3AR) having an identical N-terminal region shows similar biological profiles to TMIGD3 i1. Protein expression of TMIGD3 and A3AR is lower in human OS tissues than normal tissues. Mechanistically, TMIGD3 i1 and A3AR commonly inhibit the PKA-Akt-NF-κB axis. However, TMIGD3 i1 only partially rescues phenotypes induced by A3AR knockdown, suggesting the presence of distinct pathways. Our findings reveal an unappreciated role for TMIGD3 i1 as a suppressor of NF-κB activity and OS progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.