ArticleClinical & experimental metastasis2023
PITX1 suppresses osteosarcoma metastasis through exosomal LINC00662-mediated M2 macrophage polarization.
Article in Clinical & experimental metastasis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- From mechanism to therapy: advances in macrophage polarisation and targeted intervention in osteosarcoma.Frontiers in immunology · 2026Pooled it
- Robust and efficient annotation of cell states through gene signature scoring.Genome research · 2026Article
- Deciphering the malignant synergy: metabolic reprogramming, epigenetic circuitry, and niche remodeling in osteosarcoma-macrophage crosstalk.Frontiers in immunology · 2026Review
- Review
- The therapeutic potential of exosomes in bone cancers: osteosarcoma, chondrosarcoma, and Ewing sarcoma.Investigational new drugs · 2025Review
- LINC00662 regulates osteogenic differentiation of BMSCs and inhibits fracture healing via miR-330-3p/PTEN axis.BMC musculoskeletal disorders · 2025Article
- Arjunolic acid inhibits Wnt3a-mediated macrophage M2 polarization to suppress osteosarcoma progression.Genes & nutrition · 2025Article
- PITX1 as a grading, prognostic and tumor-infiltrating immune cells marker for chondrosarcoma: a public database-based immunoassay and tissue sample analysis.Frontiers in oncology · 2025Article
- Development of a senescence-related lncRNA signature in endometrial cancer based on multiple machine learning models.Frontiers in genetics · 2025Article
- The molecular conversations of sarcomas: exosomal non-coding RNAs in tumor's biology and their translational prospects.Molecular cancer · 2024Review
- Review
- Unveiling the contribution of tumor-associated macrophages in driving epithelial-mesenchymal transition: a review of mechanisms and therapeutic Strategies.Frontiers in pharmacology · 2024Review
- Activation of the CCL22/CCR4 causing EMT process remodeling under EZH2-mediated epigenetic regulation in cervical carcinoma.Journal of Cancer · 2024Article
- PITX1 plays essential functions in cancer.Frontiers in oncology · 2023Review
- Identification of potential key variants in mandibular premolar hypodontia through whole-exome sequencing.Frontiers in genetics · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paired-like homeodomain transcription factor 1 (PITX1) is frequently downregulated in cancers, including osteosarcoma (OS). However, its role in OS remains unknown. Therefore, we aimed to explore the functions and potential mechanisms of PITX1 in OS malignant progression. Elevated PITX1 suppressed OS cell proliferation and migration, based on transwell, proliferation, and colony formation assays. Pathway enrichment analysis of differentially-expressed genes between PITX1-overexpressing and control OS cells indicated that PITX1 expression was associated with the FAK/Src and PI3k/Akt signaling pathways. Mechanistically, ubiquitination assays and rescue experiments showed that PITX1 interacted with transcription factor STAT3, leading to decreased STAT3 transcriptional activity, which repressed the expression of LINC00662. Specific knockdown of LINC00662 reduced the tumor growth and invasion of OS cells induced by downregulated PITX1. Moreover, exosomal LINC00662, derived from PITX1 knockdown OS cell lines activated M2 macrophages in cell co-culture assays. M2 macrophage secreted several cytokines, among which CCL22 was found to cause OS cell EMT. Collectively, our data indicate that PITX1 suppresses OS cell proliferation and metastasis by downregulating LINC00662. Moreover, LINC00662 can be packaged into OS cell-derived exosomes to mediate M2 macrophage polarization to promote OS metastasis via CCL22.
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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 OpenQuestion graph.