FBLIM1

Last update 08 May 2025

Basic Info

Synonyms

CAL, FBLIM1, FBLP-1

+ [6]

Introduction

Serves as an anchoring site for cell-ECM adhesion proteins and filamin-containing actin filaments. Is implicated in cell shape modulation (spreading) and motility. May participate in the regulation of filamin-mediated cross-linking and stabilization of actin filaments. May also regulate the assembly of filamin-containing signaling complexes that control actin assembly. Promotes dissociation of FLNA from ITGB3 and ITGB7. Promotes activation of integrins and regulates integrin-mediated cell-cell adhesion.

100 Clinical Results associated with FBLIM1

100 Translational Medicine associated with FBLIM1

0 Patents (Medical) associated with FBLIM1

Literatures (Medical) associated with FBLIM1

04 Nov 2024·Journal of Cell Biology

Migfilin promotes autophagic flux through direct interaction with SNAP29 and Vamp8

Article

Author: Ding, Yanyan ; Bai, Panzhu ; Zhao, Yan G. ; Wu, Chuanyue ; Liu, Chengmin ; Xiong, Zailin ; Cai, Renwei ; Tian, Ruijun ; Yang, Aihua ; Wei, Wenjie ; Deng, Yi ; Sun, Ying ; Li, Binbin ; Quan, Meiling ; Li, Guizhen

Autophagy plays a crucial role in cancer cell survival by facilitating the elimination of detrimental cellular components and the recycling of nutrients. Understanding the molecular regulation of autophagy is critical for developing interventional approaches for cancer therapy. In this study, we report that migfilin, a focal adhesion protein, plays a novel role in promoting autophagy by increasing autophagosome–lysosome fusion. We found that migfilin is associated with SNAP29 and Vamp8, thereby facilitating Stx17-SNAP29-Vamp8 SNARE complex assembly. Depletion of migfilin disrupted the formation of the SNAP29-mediated SNARE complex, which consequently blocked the autophagosome-lysosome fusion, ultimately suppressing cancer cell growth. Restoration of the SNARE complex formation rescued migfilin-deficiency–induced autophagic flux defects. Finally, we found depletion of migfilin inhibited cancer cell proliferation. SNARE complex reassembly successfully reversed migfilin-deficiency–induced inhibition of cancer cell growth. Taken together, our study uncovers a new function of migfilin as an autophagy-regulatory protein and suggests that targeting the migfilin–SNARE assembly could provide a promising therapeutic approach to alleviate cancer progression.

16 Dec 2023·Open Medicine

FBLIM1 mRNA is a novel prognostic biomarker and is associated with immune infiltrates in glioma

Article

Author: Zeng, Kailiang ; Ling, Yunzhi ; Zhu, Gang ; Tian, Yu ; Fang, Shumin ; Zheng, Yi ; Jiang, Xiaocong ; Tu, Yanyang ; Deng, Yifan ; Wu, Diancheng

AbstractGlioma is the most common primary brain tumor. Filamin-binding LIM protein 1 (FBLIM1) has been identified in multiple cancers and is suspected of playing a part in the development of tumors. However, the potential function of FBLIM1 mRNA in glioma has not been investigated. In this study, the clinical information and transcriptome data of glioma patients were, respectively, retrieved from the TCGA and CGGA databases. The expression level of FBLIM1 mRNA was shown to be aberrant in a wide variety of malignancies. Significantly, when glioma samples were compared to normal brain samples, FBLIM1 expression was shown to be significantly elevated in the former. A poor prognosis was related to high FBLIM1 expression, which was linked to more advanced clinical stages. Notably, multivariate analyses demonstrated that FBLIM1 expression was an independent predictor for the overall survival of glioma patients. Immune infiltration analysis disclosed that FBLIM1 expression had relevance with many immune cells. The results of RT-PCR suggested that FBLIM1 expression was markedly elevated in glioma specimens. Functional experiments unveiled that the knockdown of FBLIM1 mRNA suppressed glioma cell proliferation. In general, we initially discovered that FBLIM1 mRNA might be a possible prognostic marker in glioma.

01 Jul 2023·Cancer Immunology, Immunotherapy

Integrative analyses of bulk and single-cell RNA-seq identified cancer-associated fibroblasts-related signature as a prognostic factor for immunotherapy in NSCLC

Article

Author: Fan, Guangyu ; Gao, Ruyun ; Han, Xiaohong ; Shi, Yuankai ; He, Yajun ; Li, Lin ; Wang, Shasha ; Xie, Tongji ; Yang, Mengwei ; Lou, Ning ; Dai, Liyuan

An emerging view regarding cancer-associated fibroblast (CAF) is that it plays a critical role in tumorigenesis and immunosuppression in the tumor microenvironment (TME), but the clinical significance and biological functions of CAFs in non-small cell lung cancer (NSCLC) are still poorly explored. Here, we aimed to identify the CAF-related signature for NSCLC through integrative analyses of bulk and single-cell genomics, transcriptomics, and proteomics profiling. Using CAF marker genes identified in weighted gene co-expression network analysis (WGCNA), we constructed and validated a CAF-based risk model that stratifies patients into two prognostic groups from four independent NSCLC cohorts. The high-score group exhibits a higher abundance of CAFs, decreased immune cell infiltration, increased epithelial-mesenchymal transition (EMT), activated transforming growth factor beta (TGFβ) signaling, and a limited survival rate compared with the low-score group. Considering the immunosuppressive feature in the high-score group, we speculated an inferior clinical response for immunotherapy in these patients, and this association was successfully verified in two NSCLC cohorts treated with immune checkpoint blockades (ICBs). Furthermore, single-cell RNA sequence datasets were used to clarify the molecular mechanisms underlying the aggressive and immunosuppressive phenotype in the high-score group. We found that one of the genes in the risk model, filamin binding LIM protein 1 (FBLIM1), is mainly expressed in fibroblasts and upregulated in CAFs compared to fibroblasts from normal tissue. FBLIM1-positive CAF subtype was correlated with increased TGFβ expression, higher mesenchymal marker level, and immunosuppressive tumor microenvironment. Finally, we demonstrated that FBLIM1 might serve as a poor prognostic marker for immunotherapy in clinical samples. In conclusion, we identified a novel CAF-based classifier with prognostic value in NSCLC patients and those treated with ICBs. Single-cell transcriptome profiling uncovered FBLIM1-positive CAFs as an aggressive subtype with a high abundance of TGFβ, EMT, and an immunosuppressive phenotype in NSCLC.

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FBLIM1

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