MFAP3L

Last update 08 May 2025

Basic Info

Synonyms

KIAA0626, MFAP3L, microfibril associated protein 3 like

+ [3]

Introduction

May participate in the nuclear signaling of EGFR and MAPK1/ERK2. May a have a role in metastasis.

100 Clinical Results associated with MFAP3L

100 Translational Medicine associated with MFAP3L

0 Patents (Medical) associated with MFAP3L

Literatures (Medical) associated with MFAP3L

21 Oct 2022·Clinical and Experimental Immunology

Identifying platelet-derived factors as amplifiers ofB. burgdorferi-induced cytokine production

Article

Author: Baarsma, M E ; Kerstholt, Mariska ; Lupse, Mihaela ; Oosting, Marije ; van de Schoor, Freek R ; Kischkel, Brenda ; dos Santos, Jéssica C ; van den Wijngaard, Cees C ; Tunjungputri, Rahajeng N ; Netea, Mihai G ; Jaeger, Martin ; Joosten, Leo A B ; van der Heijden, Wouter A ; Li, Yang ; Moorlag, Simone J C F M ; de Mast, Quirijn ; Hovius, Joppe W ; Vrijmoeth, Hedwig D ; Kullberg, Bart-Jan

AbstractPrevious studies have shown that monocytes can be ‘trained’ or tolerized by certain stimuli to respond stronger or weaker to a secondary stimulation. Rewiring of glucose metabolism was found to be important in inducing this phenotype. As we previously found that Borrelia burgdorferi (B. burgdorferi), the causative agent of Lyme borreliosis (LB), alters glucose metabolism in monocytes, we hypothesized that this may also induce long-term changes in innate immune responses. We found that exposure to B. burgdorferi decreased cytokine production in response to the TLR4-ligand lipopolysaccharide (LPS). In addition, B. burgdorferi exposure decreased baseline levels of glycolysis, as assessed by lactate production. Using GWAS analysis, we identified a gene, microfibril-associated protein 3-like (MFAP3L) as a factor influencing lactate production after B. burgdorferi exposure. Validation experiments proved that MFAP3L affects lactate- and cytokine production following B. burgdorferi stimulation. This is mediated by functions of MFAP3L, which includes activating ERK2 and through activation of platelet degranulation. Moreover, we showed that platelets and platelet-derived factors play important roles in B. burgdorferi-induced cytokine production. Certain platelet-derived factors, such chemokine C-X-C motif ligand 7 (CXCL7) and (C-C motif) ligand 5 (CCL5), were elevated in the circulation of LB patients in comparison to healthy individuals.

01 Apr 2016·Breast Cancer Research and TreatmentQ2 · MEDICINE

A novel gene expression signature for bone metastasis in breast carcinomas

Q2 · MEDICINE

Article

Author: van de Vijver, Marc J ; Savci-Heijink, C Dilara ; Koster, Jan ; Halfwerk, Hans

Metastatic cancer remains the leading cause of death for patients with breast cancer. To understand the mechanisms underlying the development of distant metastases to specific sites is therefore important and of potential clinical value. From 157 primary breast tumours of the patients with known metastatic disease, gene expression profiling data were generated and correlated to metastatic behaviour including site-specific metastasis, metastasis pattern and survival outcomes. We analysed gene expression signatures specifically associated with the development of bone metastases. As a validation cohort, we used a published dataset of 376 breast carcinomas for which gene expression data and site-specific metastasis information were available. 80.5 % of luminal-type tumours developed bone metastasis as opposed to 41.7 % of basal and 55.6 % of HER2-like tumours. A novel 15-gene signature identified 82.4 % of the tumours with bone metastasis, 85.2 % of the tumours which had bone metastasis as first site of metastasis and 100 % of the ones with bone metastasis only (p 9.99e-09), in the training set. In the independent dataset, 81.2 % of the positive tested tumours had known metastatic disease to the bone (p 4.28e-10). This 15-gene signature showed much better correlation with the development of bone metastases than previously identified signatures and was predictive in both ER-positive as well as in ER-negative tumours. Multivariate analyses revealed that together with the molecular subtype, our 15-gene expression signature was significantly correlated to bone metastasis status (p <0.001, 95 % CI 3.86-48.02 in the training set; p 0.001, 95 % CI 1.54-5.00 in the independent set). The 15 genes, APOPEC3B, ATL2, BBS1, C6orf61, C6orf167, MMS22L, KCNS1, MFAP3L, NIP7, NUP155, PALM2, PH-4, PGD5, SFT2D2 and STEAP3, encoded mainly membrane-bound molecules with molecular function of protein binding. The expression levels of the up-regulated genes (NAT1, BBS1 and PH-4) were also found to be correlated to epithelial to mesenchymal transition status of the tumour. We have identified a novel 15-gene expression signature associated with the development of bone metastases in breast cancer patients. This bone metastasis signature is the first to be identified using a supervised classification approach in a large series of patients and will help forward research in this area towards clinical applications.

01 Sep 2014·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

MFAP3L activation promotes colorectal cancer cell invasion and metastasis

Article

Author: Lu, Youyong ; Hao, Chunyi ; Kang, Bin ; Liu, Siqi ; Lou, Xiaomin ; Tian, Xiuyun ; Zhang, Jun ; Xu, Ningzhi ; Li, Wenmei

An abundance of microfibril-associated glycoprotein 3-like (MFAP3L) significantly correlates with distant metastasis in colorectal cancer (CRC), although the mechanism has yet to be explained. In this study, we observed that MFAP3L knock-down resulted in reduced CRC cell invasion and hepatic metastasis. We evaluated the cellular location and biochemical functions of MFAP3L and found that this protein was primarily localized in the nucleus of CRC cells and acted as a protein kinase. When EGFR translocated into the nucleus upon stimulation with EGF, MFAP3L was phosphorylated at Tyr287 within its SH2 motif, and the activated form of MFAP3L phosphorylated ERK2 at Thr185 and Tyr187. Moreover, the metastatic behavior of CRC cells in vitro and in vivo could be partially explained by activation of the nuclear ERK pathway through MFAP3L phosphorylation. Hence, we experimentally demonstrated for the first time that MFAP3L likely participates in the nuclear signaling of EGFR and ERK2 and acts as a novel nuclear kinase that impacts CRC metastasis.

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MFAP3L

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