ArticleAmerican journal of cancer research2021
DLX5 promotes osteosarcoma progression via activation of the NOTCH signaling pathway.
Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Long non-coding RNA PRSS23-AS1 as ceRNA promotes breast cancer progression by regulating EMT via miR-3176 /YBX1 axis.Cancer gene therapy · 2025Article
- DLX2 promotes gastric cancer epithelial- mesenchymal transition and malignant progression through the PI3K/AKT signaling pathway.Frontiers in oncology · 2025Article
- New direction: identification of immunoinflammatory subtypes and potential therapeutic targets for cholangiocarcinoma.Discover oncology · 2024Article
- FGL1 Promotes Tumor Immune Escape in Stomach Adenocarcinoma via the Notch Signaling Pathway.Molecular biotechnology · 2024Article
- Expression profile of long noncoding RNAs and comprehensive analysis of lncRNA-cisTF-DGE regulation in condyloma acuminatum.BMC medical genomics · 2024Article
- Long non-coding RNA RP11-197K6.1 as ceRNA promotes colorectal cancer progression via miR-135a-5p/DLX5 axis.Journal of translational medicine · 2024Article
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- MFNG is an independent prognostic marker for osteosarcoma.European journal of medical research · 2023Article
- Comprehensive analysis of distal-less homeobox family gene expression in colon cancer.World journal of gastrointestinal oncology · 2023Article
- SHFM1 deficiency suppresses esophageal squamous cell carcinomas progression via modulating NF‑κB signaling and enhancing nature killer cell‑mediated tumor surveillance.Experimental and therapeutic medicine · 2023Article
- Article
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- The molecular mechanism research of cartilage calcification induced by osteoarthritis.Bioengineered · 2022Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The distal-less (dlx) homeobox transcription factors have been implicated roles in bone development. DLX5, in particular, was shown to play essential roles in osteoblast differentiation by targeting RUNX2, a master transcription factor for bone development. Interestingly, DLX5 has also been shown to play an oncogenic role in lung and other cancers, possibly via regulation of MYC expression. Given its dual roles in bone and cancer, this study aimed to investigate the effect of DLX5 on progression of osteosarcoma (OS), the primary bone cancer that is characterized by abnormal bone formation and osteoblast activity. Expression of DLX5 in OS cell lines was detected by quantitative real-time PCR (qRT-PCR) and western blot (WB). In vitro and in vivo assays were performed to investigate the oncogenic function of DLX5 in OS cells and xenograft models. Luciferase reporter assay was performed to determine the underlying mechanism of DLX5-mediated OS aggressiveness. The results showed that DLX5 was differentially expressed in OS cell lines, with significantly upregulated levels in HOS and MG-63 and relatively low levels in U2OS and 143B cell lines, compared with the normal bone cell line. DLX5 knockdown in HOS and MG-63 cell lines by siRNA inhibited OS cell growth and progression, and induced cell apoptosis and cell cycle changes both in vitro and in vivo. Meanwhile, DLX5 overexpression had the opposite effect on U2OS and 143B cell lines. Notably, a positive correlation between the expression patterns of NOTCH1 and DLX5 was also observed. The expression levels of NICD (NOTCH1 intracellular domain) and HES1 (classical target of NOTCH) were closely associated with DLX5 expression. Whereas knockdown of DLX5 in OS cells resulted in decreased expression of NOTCH1 and reduced cell proliferation and migration, which were rescued by overexpression of NOTCH1. We further analyzed DLX5 and NOTCH1 genes using JASPAR software and found two potential DLX5 binding sites within the
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Identifiers
34249467PMC8263696W3180021894What Socratic holds
Registered trials
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 Socratic graph.