Ask about this productRelated genes to: VGLL3 Blocking Peptide
- Gene:
- VGLL3 NIH gene
- Name:
- vestigial like family member 3
- Previous symbol:
- -
- Synonyms:
- VGL-3
- Chromosome:
- 3p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-30
- Date modifiied:
- 2015-11-23
Related products to: VGLL3 Blocking Peptide
Related articles to: VGLL3 Blocking Peptide
- Vestigial-like family member 3 (VGLL3), a transcriptional cofactor of the TEA domain family, has been previously identified as a regulator of osteoblast differentiation. Building upon our previous findings, we investigated VGLL3 function in MC3T3-E1 osteoblasts using an integrated approach combining transcriptomic analysis and functional assays to identify its downstream effectors and explore associated autophagy mechanisms. RNA-seq analysis of Vgll3-knockdown (shVgll3) cells identified death-associated protein kinase 2 (DAPK2), a regulator of autophagy, as a downstream effector. Autophagic activity was examined using transmission electron microscopy and western blot analysis of LC3-II and p62 proteins. The effects of Dapk2 knockdown (shDapk2) on osteoblast differentiation were evaluated using qPCR, western blotting, alkaline phosphatase staining, and Alizarin Red staining. Rapamycin treatment was used to determine whether pharmacologic activation of autophagy could restore osteoblast function. Vgll3 knockdown significantly suppressed autophagic flux, as evidenced by fewer autophagic vacuoles, decreased LC3-II accumulation, and increased p62 expression. A comparable reduction in autophagic activity was observed in shDapk2 cells and was accompanied by impaired osteoblast differentiation. Rapamycin treatment partially restored autophagy and osteogenic differentiation in Vgll3-deficient cells. Finally, overexpression of DAPK2 partially rescued autophagic activity and osteogenic differentiation in shVgll3 cells, supporting its role as a key downstream functional effector. FOXM1 was further implicated as a potential transcriptional regulator contributing to DAPK2 expression. Collectively, our findings suggest that VGLL3 may influence osteogenic differentiation in osteoblasts, potentially involving DAPK2-associated autophagy. - Source: PubMed
He YuhanWang ZiyiWeng YaoSitosari HeriatiZheng YilinQu YaxinIkegame MikaOkamura Hirohiko - Cellular plasticity plays essential roles in development including organogenesis and tissue homeostasis. The epithelial-to-mesenchymal transition (EMT) is no longer considered a binary switch but rather a dynamic process characterized by a continuum of metastable intermediates having unique features. This epithelial-mesenchymal (E/M) plasticity can be co-opted by cancer cells to promote dedifferentiation that results in hybrid E/M states which increase tumor heterogeneity and generate distinct molecular and phenotypic adaptations that promote drug resistance, dormancy, recurrence, and/or cell invasion and metastasis. The mechanisms that coordinate and maintain metastable hybrid E/M states are poorly understood, and here we report they are controlled by the master transcription factor CREB which regulates adaptive response genes necessary for E/M plasticity. Specifically, a CREB-dependent head and neck cancer model validated the role of CREB in cancer cell plasticity and revealed that it controls a non-canonical EMT gene signature. Moreover, analyses of this signature across cancer types identified the transcriptional regulators VGLL3 and KLF3 as core PanCancer mediators of hybrid E/M states, and gain- and loss-of-function studies established that CREB regulates E/M plasticity by coordinating VGLL3 and KLF3 to drive metastasis. - Source: PubMed
Publication date: 2025/12/11
Parag-Sharma KshitijBharambe HarishPowers John JGong WeidaPurcell Daniel JMensah CalebTwomey ChloeMehta Jay HLamouille SamyAmelio Antonio L - Recently, a distinct, bland spindle cell neoplasm with rhabdomyoblastic phenotype, and VGLL3 rearrangement has been described. These tumors have a striking predilection for the head and neck area and so far, followed an indolent course. It remains unclear whether these tumors are best classified as true rhabdomyosarcomas. There are 11 reports of such tumors with limited follow-up. Here, we report an additional case with local recurrence, long-term follow-up and spatial profiling. The tumor occurred in the right buccal mucosa/oral commissure of a 47-year-old man. On clinical examination, the mass was firm, measuring ~1.5 cm. Biopsy and subsequent wedge excision were performed. Histologically, the tumor was composed of bland, small, spindle to ovoid cells, arranged in short fascicles and vaguely storiform architecture. The tumor cells diffusely infiltrated into skeletal muscle. There was a background of inflammatory cells including small lymphocytes and histiocytes. Neoplastic cells were positive for SMA, demsin, PAX7, myogenin and MyoD1. Whole transcriptome sequencing revealed a TCF12::VGLL3 fusion. Digital spatial profiling (DSP) identified pan-AKT expression, differential expression in the MAPK pathway, and revealed that the tumor attracted a dense T-cell rich inflammatory infiltrate. The patient had a lesion in the same location 6 years prior that underwent incisional biopsy, showed intense inflammatory infiltrate, and was interpreted as benign. FISH for VGLL3 on this tissue was positive for rearrangement. No additional adjuvant treatment was given, and the patient is alive without disease, 8 months after the major resection. Long term follow-up of 6 years with only local recurrence lends further support to the notion that these neoplasms are a class of indolent/low-grade rhabdomyoblastic tumors that are biologically and clinically distinct from fully malignant spindle cell rhabdomyosarcomas. - Source: PubMed
Dashti Nooshin KChakraborty DebopriyaSadanandappa Madhumala KDehner Carina AZhang Paul JPaydarfar Joseph ATafe Laura J - Preeclampsia affects approximately 1 in 10 pregnancies, leading to severe complications and long-term health risks for both mother and offspring. While the etiology remains unclear, preeclampsia has been linked to both autoimmunity and the timing of menarche. - Source: PubMed
Publication date: 2026/04/09
Plazyo OlesyaChopp Laura BPeela RishyanthYoung KellyZhang HaihanBogle RachaelHesson AshleyLangen Elizabeth SBergin Ingrid LSyu Li-JyunErba JakeKirma JosephDey PoulamiZhang LinSarkar Mrinal KSwindell William RGallagher Katherine AWard Nicole LSinger KanakadurgaKahlenberg J MichelleBilli Allison CDlugosz Andrzej AGanesh Santhi KTsoi Lam CGudjonsson Johann E - Insufficient T-cell infiltration limits the effectiveness of immunotherapy in sarcoma, yet the tumor-intrinsic mechanisms that govern immune exclusion remain poorly defined. - Source: PubMed
Publication date: 2026/04/01
Cruz De Los Santos MireiaChen YiGonzález De Zárate AmaiaSorteberg AgnesZhao HongleiVázquez-Cabrera GuillermoBigdeli NedaKolbeinsdottir SolrunMannion AarrenBaldran-Groves LucasNeo Shi YongWickström Stina LinneaMelief JeroenHolmgren LarsHerold NikolasHaglund de Flon FelixLundqvist Andreas