ArticleBiochemical and biophysical research communications2017
ALG2 regulates glioblastoma cell proliferation, migration and tumorigenicity.
Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
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- WZY-321 triggers glioma cell apoptosis via XAF1 up-regulation caused by MTM-mediated miR-873 down-regulation.Journal of Cancer · 2022Article
- Structural insights into the recognition of histone H3Q5 serotonylation by WDR5.Science advances · 2021Article
- miRNAs Involved in Esophageal Carcinogenesis and miRNA-Related Therapeutic Perspectives in Esophageal Carcinoma.International journal of molecular sciences · 2021Review
- Transient Receptor Potential (TRP) Ion Channels Involved in Malignant Glioma Cell Death and Therapeutic Perspectives.Frontiers in cell and developmental biology · 2021Review
- PDCD6 cooperates with C-Raf to facilitate colorectal cancer progression via Raf/MEK/ERK activation.Journal of experimental & clinical cancer research : CR · 2020Article
- Transient Receptor Potential Mucolipin-1 Channels in Glioblastoma: Role in Patient's Survival.Cancers · 2019Article
- TROP2 promotes the proliferation and metastasis of glioblastoma cells by activating the JAK2/STAT3 signaling pathway.Oncology reports · 2019Article
- microRNA-124-3p inhibits the progression of congenital hypothyroidism via targeting programmed cell death protein 6.Experimental and therapeutic medicine · 2018Article
- Article
- Association between single nucleotide polymorphisms in the programmed cell death 6 gene and the risk of endometrial cancer in Chinese Han women.International journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Apoptosis-linked gene-2 (ALG-2), also known as programmed cell death 6 (PDCD6), has recently been reported to be aberrantly expressed in various tumors and required for tumor cell viability. The aim of the present study was to investigate whether ALG-2 plays a crucial role in tumor cell proliferation, migration and tumorigenicity. In this study, we examined the expression of PDCD6 in glioblastoma cell lines and found that ALG-2 was generally expressed in glioblastoma cell lines. We also performed an analysis of an online database and found that high expression of ALG-2 was associated with poor prognosis (p = 0.039). We found that over-expression of ALG2 in glioblastoma could inhibit cell proliferation and, conversely, that down-regulation of ALG2 could promote cell proliferation. Further studies showed that over-expression of ALG2 inhibited the migration of tumor cells, whereas down-regulation of ALG2 promoted tumor cell migration. Finally, in vitro and in vivo studies showed that over-expression of ALG2 inhibited the tumorigenic ability of tumor cells, while down-regulation of ALG2 promoted tumor cell tumorigenic ability. In conclusion, ALG2 has a tumor suppressive role in glioblastoma and might be a potential target for the treatment of glioblastoma.
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