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Last update 08 May 2025

MYOF

Last update 08 May 2025

Basic Info

Synonyms

Fer-1-like protein 3, FER1L3, KIAA1207

+ [2]

Introduction

Calcium/phospholipid-binding protein that plays a role in the plasmalemma repair mechanism of endothelial cells that permits rapid resealing of membranes disrupted by mechanical stress. Involved in endocytic recycling. Implicated in VEGF signal transduction by regulating the levels of the receptor KDR (By similarity).

Drugs associated with MYOF

WJ-460

Target

MYOF

Mechanism

MYOF inhibitors

Active Org.

East China Normal University

Originator Org.

East China Normal University

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

HJ445A

Target

MYOF

Mechanism

MYOF inhibitors

Active Org.

East China Normal University

Originator Org.

East China Normal University

Active Indication

Stomach Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MYOF

100 Translational Medicine associated with MYOF

0 Patents (Medical) associated with MYOF

208

Literatures (Medical) associated with MYOF

01 Apr 2025·Neoplasia

Exogenous BMI1 expression aggravates oral squamous cell carcinomas in tongue epithelia

Article

Author: Baquero, Jorge ; Chen, Qiuying ; Miller, Dawson ; Zhang, Tuo ; Gross, Steven ; Tang, Xiao-Han ; Gudas, Lorraine J ; Scognamiglio, Theresa ; Galke, Daniel

Oral squamous cell carcinoma (OSCC) is characterized by aggressiveness and a poor prognosis, in part because most patients are diagnosed during the later stages of the disease. B cell-specific Moloney murine leukemia virus integration site 1 (BMI1), part of polycomb repressive complex 1 (PRC1), is a key transcription factor overexpressed in OSCC. Although increased BMI1 has been linked to tumor formation in mouse models of the disease, the molecular mechanisms have not been elucidated. Here we used a transgenic mouse line (KrTB) that selectively overexpresses BMI1 in the tongue basal epithelial stem cells (SCs) to delineate BMI1 actions during oral tumorigenesis. By tumor pathological classification after 4-nitroquinoline 1-oxide (4-NQO)-induced carcinogenesis we detected more severe tumors in mice with ectopic BMI1 expression. Genome-wide transcriptomics indicated that mRNAs associated with human OSCC, including SOX9, HIF1A, MMP9, INHBB, and MYOF, were further increased by ectopic BMI1 expression in murine tongue epithelia. mRNAs encoding multiple metabolic targets, such as SLC2A1 (GLUT1), PKM, LDHA, and HK2, were also increased upon BMI1 overexpression in 4-NQO-treated tongue epithelia. Furthermore, we detected BMI1, SOX9, and GLUT1 proteins in the infiltrating cells of invasion fronts identified by markers of invasive SCCs. Finally, metabolomic data show that BMI1 overexpression in tongue epithelia promotes glycolysis during 4-NQO-induced carcinogenesis. Thus, our data demonstrate that BMI1 causes OSCC cells to alter cell metabolism, as changes in many of these transcripts are linked to increased glycolysis and metabolic reprograming that occurs during carcinogenesis.

01 Feb 2025·Current Opinion in Allergy & Clinical Immunology

Exploring the management of recurrent angioedema caused by different mechanisms

Review

Author: Mormile, Ilaria ; Suffritti, Chiara ; Bova, Maria

Purpose of reviewWe aim to explore the most recent insights into the pathogenesis of recurrent angioedema caused by different mechanisms and then focus on the management and treatment approaches available.Recent findingsThe recently developed DANCE consensus classification identifies five types of angioedema: mast cell-mediated (AE-MC), bradykinin-mediated, because of intrinsic vascular endothelium dysfunction (AE-VE), drug-induced (AE-DI), and due to unknown mechanisms (AE-UNK). These subtypes require different management with treatment choices targeting the main pathogenetic pathways involved in each form. For AE-MC and AE-BK, the therapeutic landscape has been significantly widened in recent years. Conversely, there is a lack of consensus for the hereditary forms because of newly discovered mutations (factor 12, plasminogen, kininogen-1, myoferlin, angiopoietin-1, heparan sulfate 3-O-sulfotransferase 6) and AE-UNK.SummaryRecurrent angioedema can present with or without wheals. Angioedema without wheals may be driven by bradykinin and/or mast cell mediators. The different forms respond to specific drugs and require a different management. For its potentially life-threatening and disfiguring features, angioedema should be promptly recognized and effectively treated. For this reason, enhancing awareness about various angioedema subtypes and their management provide a useful tool for the clinical practice.

01 Feb 2025·Cancer Letters

hnRNPLL regulates MYOF alternative splicing and correlates with early metastasis in pancreatic ductal adenocarcinoma

Article

Author: Yu, Qian ; Lei, Ke ; Sun, Mingyue ; Chen, Xianghan ; Wang, Jigang ; Liu, Xiaolan ; Wang, Lili ; Gong, Ruining ; Ren, He ; Saluja, Ashok Kumar

Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer known for its high rate of early metastasis, necessitating the discovery of the underlying mechanisms. Herein, we report that heterogeneous nuclear ribonucleoprotein L-like (hnRNPLL) expression significantly increases at the invasion forefront in PDAC and is associated with early metastasis and poor prognosis. Our findings revealed that hnRNPLL knockdown resulted in extensive exon skipping (ES) events. In particular, we identified myoferlin (MYOF), a member of the ferlin family involved in membrane processes, as a functional splicing target of hnRNPLL. hnRNPLL depletion stimulates MYOF exon 17 retention to reduce the short isoform of MYOF (MYOFb) and inhibit metastasis. In contrast, hnRNPLL or MYOFb overexpression promoted pancreatic cancer cell migration and invasion. These results suggest that hnRNPLL is a critical factor for early PDAC metastasis. hnRNPLL and MYOFb may be potential therapeutic targets for PDAC.

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MYOF

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