Differential expression of filamin B splice variants in giant cell tumor cells

Tsui, J; Lau, Carol; Cheung, Alex Chun; Wong, Kwok-Chuen; Huang, Lin; Tsui, Stephen Kwok-Wing; Kumta, S. M.

doi:10.3892/or.2016.5197

Cited by 5 publications

(3 citation statements)

References 28 publications

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“…Recently, FLNB has been considered one of the biomarkers for cancer. Splicing variants of FLNB expression have been reported to play key roles in the proliferation and differentiation of tumor cells (33). A recent study demonstrated that in HMLE cells (immortalized human mammary epithelial cells), FLNB interacts with forkhead box C1 (FOXC1) to form a complex (11).…”

Section: Discussionmentioning

confidence: 99%

Filamin B extensively regulates transcription and alternative splicing, and is associated with apoptosis in HeLa cells

Cao

Wang

et al. 2020

Oncol Rep

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Post-transcriptional mechanisms are an important approach in the treatment of cancer, and may also be hijacked by tumor cells to help adapt to the local microenvironment. Filamin B (FLNB), an actin-binding protein that provides crucial scaffolds for cell motility and signaling, has also been identified as an RNA-binding protein. Recent studies demonstrated that FLNB might play an important role, not only in skeletal development, but also in regulating tumorigenesis; however, the effects of dysregulated expression of FLNB at the molecular level are not clear. In the present study, RNA-sequencing was performed to analyze changes in overall transcriptional and alternative splicing between the knocked-down FLNB and the control in HeLa cells. Decreased FLNB levels resulted in significantly lower apoptosis compared with control cells. FLNB knockdown extensively regulated the expression of genes in cell apoptosis, tumorigenesis, metastases, transmembrane transport and cartilage development. Moreover, FLNB regulated alternative splicing of a large number of genes involved in 'cell death' and the 'apoptotic process'. Some genes and alternative splicing related to skeletal development were enriched and regulated by FLNB. Reverse transcription-quantitative-PCR identified FLNB-regulated transcription and alternative splicing of genes, such as NLR family apoptosis inhibitory protein, interleukin 23 subunit α, metastasis associated lung adenocarcinoma transcript 1, phosphofurin acidic cluster sorting protein 2, bone morphogenetic protein 7, matrix metallopeptidase 13, collagen type II α 1 chain, fibroblast growth factor receptor 2 and vitamin D receptor. The present study is the first study, to the best of the authors' knowledge, to provide transcriptome-wide analysis of differential gene expression and alternative splicing upon FLNB silencing. The present results suggested that FLNB may play an important regulatory role in cervical cancer cell apoptosis via regulation of transcription and alternative splicing, which provide insight for the current understanding of the mechanisms of FLNB-mediated gene regulation.

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Section: Discussionmentioning

confidence: 99%

Filamin B extensively regulates transcription and alternative splicing, and is associated with apoptosis in HeLa cells

Cao

Wang

et al. 2020

Oncol Rep

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“…FLNB (Filamin B) is a cytoskeletal protein encoded by the gene on autosomal chromosome 3. It is cross-linked with actin to form a three-dimensional cytoskeletal network and maintain cell morphology (Tsui et al 2016;Devis et al 2017). FLNB is involved in many physiological and biochemical activities, including transcriptional regulation and cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

Interaction between LncRNA-ROR and miR-145 contributes to epithelial-mesenchymal transition of ovarian cancer cells

Zhang²,

Wu³

et al. 2019

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Emerging evidence has indicated that long noncoding RNAs (LncRNAs) play critical roles in tumor development. LncRNA-regulator of reprogramming (ROR) could enhance the malignance of numerous tumors through promoting cell reprogramming and the chemoresistance of several cancers. Nevertheless, the detailed molecular mechanisms of LncRNA-ROR in ovarian cancer are not well elucidated. In our study, we demonstrated that LncRNA-ROR was high expression in ovarian cancer tissues than in normal ovarian tissues, and LncRNA-ROR level was positively associated with clinical stages and the differentiation grades of malignant cells. Functionally, LncRNA-ROR could induce epithelial-mesenchymal transition (EMT), and regulated ovarian cancer cell migration and invasion by decreasing the expression of tumor suppressive miR-145 and its target gene FLNB. Moreover, the binding site for miR-145 within LncRNA-ROR contributed to the reciprocal negative regulation of LncRNA-ROR and miR-145. Taken together, LncRNA-ROR promoted EMT by the miR-145/FLNB regulatory axis in ovarian cancer, providing a potential therapeutic target for ovarian cancer.

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“…It has a key role in skeletal development and its pathogenic mutations are the solely cause of skeletal deformities (26). Recently, Tsui et al reported that differential expression of Filamin B splicing variants may play a key role in proliferation and differentiation of giant cell tumor of bone (27). Another intriguing study identified Filamin B in human sera as a potential biomarker for prostate cancer (28).…”

Section: Discussionmentioning

confidence: 99%

Filamin B and CD13 are components of senescent secretomes that may be involved in primary (stress induced) and paracrine senescence of mesenchymal stromal cells

Squillaro¹

2019

Erciyes Med J

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Objective: In the present study we aim to evaluate whether some of the proteins previously identified in the secretome of senescent bone marrow (BM)-and adipose (A)-mesenchymal stromal cells (MSCs) could be involved in regulation of senescence phenomena. Materials and Methods:Among the identified proteins, we selected Filamin B (FLNB) and Aminopeptidase N (CD13) that were exclusively found in the secretome of senescent cells. We silenced their mRNA expression in BM-MSCs by means of RNA interference technology and induced acute senescence by hydrogen peroxide treatment. Our goal was to evaluate if FLNB or CD13 silencing may affect onset of senescence. Results:Our preliminary data showed that CD13 protein could be a key factor involved in the regulation and determination of both primary and paracrine induced senescence in human BM-MSCs. On the other hand, Filamin B seems not to be involved in the determination of primary senescence whereas its presence could be part of the mechanism that regulates the senescence induction in human BM-MSCs by paracrine signaling. Conclusion:Our study provides a useful base for identifying the complex extracellular protein networks involved in the regulation of MSC cellular senescence.

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Differential expression of filamin B splice variants in giant cell tumor cells

Cited by 5 publications

References 28 publications

Filamin B extensively regulates transcription and alternative splicing, and is associated with apoptosis in HeLa cells

Filamin B extensively regulates transcription and alternative splicing, and is associated with apoptosis in HeLa cells

Interaction between LncRNA-ROR and miR-145 contributes to epithelial-mesenchymal transition of ovarian cancer cells

Filamin B and CD13 are components of senescent secretomes that may be involved in primary (stress induced) and paracrine senescence of mesenchymal stromal cells

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