ArticleInternational journal of molecular medicine2015
Downregulation of ubiquitin-associated protein 2-like with a short hairpin RNA inhibits human glioma cell growth in vitro.
Article in International journal of molecular medicine, 2015. 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, 28 citations in OpenAlex.
- Review
- CALCOCO2 silencing represents a potential molecular therapeutic target for glioma.Archives of medical science : AMS · 2025Article
- UBAP2L contributes to formation of P-bodies and modulates their association with stress granules.The Journal of cell biology · 2024Article
- UBAP2L ensures homeostasis of nuclear pore complexes at the intact nuclear envelope.The Journal of cell biology · 2024Article
- Whole-exome sequencing identified a novel heterozygous variant inFrontiers in genetics · 2024Article
- PCK1 activates oncogenic autophagy via down-regulation Serine phosphorylation of UBAP2L and antagonizes colorectal cancer growth.Cancer cell international · 2023Article
- UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway.Cell death discovery · 2022Article
- Ubiquitin Binding Protein 2-Like (UBAP2L): is it so NICE After All?Frontiers in cell and developmental biology · 2022Review
- Stress granules in colorectal cancer: Current knowledge and potential therapeutic applications.World journal of gastroenterology · 2020Review
- MicroRNA-19a-3p inhibits the cellular proliferation and invasion of non-small cell lung cancer by downregulating UBAP2L.Experimental and therapeutic medicine · 2020Article
- UBAP2L arginine methylation by PRMT1 modulates stress granule assembly.Cell death and differentiation · 2020Article
- Knockdown of Ubiquitin Associated Protein 2-Like (UBAP2L) Inhibits Growth and Metastasis of Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer.Breast cancer (Tokyo, Japan) · 2018Article
- Comprehensive molecular biomarker identification in breast cancer brain metastases.Journal of translational medicine · 2017Article
- Ubiquitin Associated Protein 2-Like (UBAP2L) Overexpression in Patients with Hepatocellular Carcinoma and its Clinical Significance.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Depletion of UBA protein 2-like protein inhibits growth and induces apoptosis of human colorectal carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Clinical Significance of Ubiquitin-associated Protein 2-like in Patients With Uterine Cervical Cancer.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ubiquitin-associated protein 2-like (UBAP2L), which contains a ubiquitin-associated (UBA) domain near its N-terminus, has been indicated in the pathogenesis of several human cancers, including multiple myeloma, hepatocellular carcinoma and malignant ovarian tumors. However, the role of UBAP2L in human glioma remains unknown. In the present study, UBAP2L was widely expressed in multiple glioma cell lines. To further examine the effects of UBAP2L on glioma growth, lentivirus‑mediated short hairpin RNA (shRNA) was employed to knockdown UBAP2L expression in the glioblastoma cell lines. Depletion of UBAP2L significantly inhibited the proliferation and colony formation ability, as determined by MTT and colony formation assays. Cell cycle analysis showed that UBAP2L knockdown induced G0/G1 phase arrest in U251 and U373 cells, while S phase arrest was induced in A172 cells. These results suggest that UBAP2L has a key role in glioma cell growth, and may act as an oncogene to promote malignant glioma development.
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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.