ArticleOncotarget2017
Gαi3 nuclear translocation causes irradiation resistance in human glioma cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Origin recognition complex 6 overexpression promotes growth of glioma cells.Cell death & disease · 2024Article
- Identification of the central role of RNA polymerase mitochondrial for angiogenesis.Cell communication and signaling : CCS · 2024Article
- The requirement of the mitochondrial protein NDUFS8 for angiogenesis.Cell death & disease · 2024Article
- The mitochondrial protein TIMM44 is required for angiogenesis in vitro and in vivo.Cell death & disease · 2023Article
- G protein inhibitory α subunit 2 is a molecular oncotarget of human glioma.International journal of biological sciences · 2023Article
- EID3 Promotes Glioma Cell Proliferation and Survival by Inactivating AMPKα1.Journal of Korean Neurosurgical Society · 2022Article
- TIMM44 is a potential therapeutic target of human glioma.Theranostics · 2022Article
- LncRNA DGCR5 plays a tumor-suppressive role in glioma via the miR-21/Smad7 and miR-23a/PTEN axes.Aging · 2020Article
- Article
- Lnc-THOR silencing inhibits human glioma cell survival by activating MAGEA6-AMPK signaling.Cell death & disease · 2019Article
- microRNA-200a downregulation in human glioma leads to Gαi1 over-expression, Akt activation, and cell proliferation.Oncogene · 2018Article
- Antidepression action of BDNF requires and is mimicked by Gαi1/3 expression in the hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Gαi1 and Gαi3mediate VEGF-induced VEGFR2 endocytosis, signaling and angiogenesis.Theranostics · 2018Article
- SphK2 over-expression promotes osteosarcoma cell growth.Oncotarget · 2017Article
- Article
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Authors and funding
10 authors.
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Abstract
We have previously shown that Gαi3 is elevated in human glioma, mediating Akt activation and cancer cell proliferation. Here, we imply that Gαi3 could also be important for irradiation resistance. In A172 human glioma cells, Gαi3 knockdown (by targeted shRNAs) or dominant-negative mutation significantly potentiated irradiation-induced cell apoptosis. Reversely, forced over-expression of wild-type or constitutively-active Gαi3 inhibited irradiation-induced A172 cell apoptosis. Irradiation in A172 cells induced Gαi3 translocation to cell nuclei and association with local protein DNA-dependent protein kinase (DNA-PK) catalytic subunit. This association was important for DNA damage repair. Gαi3 knockdown, depletion (using Gαi3 knockout MEFs) or dominant-negative mutation potentiated irradiation-induced DNA damages. On the other hand, expression of the constitutively-active Gαi3 in A172 cells inhibited DNA damage by irradiation. Together, these results indicate a novel function of Gαi3 in irradiation-resistance in human glioma cells.
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