FERMT3 contributes to glioblastoma cell proliferation and chemoresistance to temozolomide through integrin mediated Wnt signaling

Lu, Chunhe; Cui, Chengzhi; Liu, Bo; Zou, Shufang; Song, Hongwei; Tian, Hongfei; Zhao, Juan; Li, Yan

doi:10.1016/j.neulet.2017.07.057

Cited by 28 publications

(36 citation statements)

References 39 publications

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“…ACTN2 is an F-actin cross-linking protein that participates in cell adhesion, MAPK cascade, apoptosis, and the regulation of NMDA receptor activity [ 31 ]. FERMT3 is an integrin-binding protein that plays a part in cell adhesion and activation of the integrin-mediated signaling pathway [ 32 ]. NEFL is an intermediate filament protein that maintains neuronal caliber essential for sensorimotor function and spatial orientation [ 33 ].…”

Section: Resultsmentioning

confidence: 99%

Identification of contributing genes of Huntington’s disease by machine learning

et al. 2020

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Background Huntington’s disease (HD) is an inherited disorder caused by the polyglutamine (poly-Q) mutations of the HTT gene results in neurodegeneration characterized by chorea, loss of coordination, cognitive decline. However, HD pathogenesis is still elusive. Despite the availability of a wide range of biological data, a comprehensive understanding of HD’s mechanism from machine learning is so far unrealized, majorly due to the lack of needed data density. Methods To harness the knowledge of the HD pathogenesis from the expression profiles of postmortem prefrontal cortex samples of 157 HD and 157 controls, we used gene profiling ranking as the criteria to reduce the dimension to the order of magnitude of the sample size, followed by machine learning using the decision tree, rule induction, random forest, and generalized linear model. Results These four Machine learning models identified 66 potential HD-contributing genes, with the cross-validated accuracy of 90.79 ± 4.57%, 89.49 ± 5.20%, 90.45 ± 4.24%, and 97.46 ± 3.26%, respectively. The identified genes enriched the gene ontology of transcriptional regulation, inflammatory response, neuron projection, and the cytoskeleton. Moreover, three genes in the cognitive, sensory, and perceptual systems were also identified. Conclusions The mutant HTT may interfere with both the expression and transport of these identified genes to promote the HD pathogenesis.

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Section: Resultsmentioning

confidence: 99%

Identification of contributing genes of Huntington’s disease by machine learning

et al. 2020

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“…Interestingly, FERM3 (also known as kindlin‐3) activates integrin‐mediated Wnt/β‐catenin signaling to enhance glioma cell proliferation and TMZ‐induced chemoresistance (C. Lu et al, ). Recently, tripartite motif‐containing 14 (TRIM14) also causes in chemoresistance by TMZ of glioma cells in vitro and in vivo through activating Wnt/β‐catenin cascade (Z. Tan et al, ).…”

Section: Oncogenic Effect Of Wnt/β‐catenin Signaling In Glioma Progrementioning

confidence: 99%

“…Moreover, DANCR (J. Li & Zhou, 2018) and AB073614 (C. Lu et al, 2017) positively affects glioma progression via activating Wnt/β-catenin signaling. Consistently, lncRNA NEAT1 induced by EGFR contributes to glioma development through Wnt/β-catenin cascade (Q.…”

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confidence: 99%

Wnt/β‐catenin signaling cascade: A promising target for glioma therapy

Zhou

Zeng

et al. 2018

Journal Cellular Physiology

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Glioma is one of the most treatment‐refractory intracranial tumors, and the aberrant expressed Wnt/β‐catenin pathway is closely associated with glioma malignancy. In this regard, Wnt/β‐catenin signaling has been reported to play an essential role in cellular proliferation, migration, invasion, and angiogenesis, therefore contributing to glioma progression. However, the underlying mechanisms of Wnt/β‐catenin signaling involvement in gliomagenesis remain unknown. Here, we present an overview of the Wnt components and then go on to summarize the current knowledge describing the multitude of roles of Wnt/β‐catenin in glioma, which are mediated by transcription factors, microRNAs, long noncoding RNAs, and so on. In the latter portion of the review, we elaborate the increasing apparent crosstalk of Wnt/β‐catenin pathway with PI3K/AKT signaling involved in these processes. Ultimately, compounds targeting the Wnt/β‐catenin are described in glioma. As better understanding of the regulatory mechanisms to glioma malignancies increases, Wnt/β‐catenin cascade may represent an area of developmental glioma therapeutics focus.

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“…However, independent evidence for the role of kindlin-3 in BC can be taken from interrogation of the Oncomine database (http://www.oncomine.com) in which kindlin-3 ranked in the top 3% of up-regulated genes. Furthermore, in glioblastoma, kindlin-3 contributed to resistance to telozolomide and cell proliferation through Wnt signaling (Lu et al, 2017), whereas overexpression of kindlin-3 in melanoma cells led to imbalanced Rho GTP-ase activation and inhibition of cell migration (Feng et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Site-specific phosphorylation regulates the functions of kindlin-3 in a variety of cells

et al. 2019

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Studies of isolated cells, mice, and humans have demonstrated the vital role of the FERM domain protein kindlin-3 in integrin activation in certain hematopoietic and non-hematopoietic cells, consequent to binding to integrin β-subunits. To explore regulatory mechanisms, we developed a monoclonal antibody that selectively recognizes the phosphorylated form of Ser484 (pS484) in kindlin-3. Activation of platelets, HEL megakaryocytic-like cells and BT549 breast cancer cells led to enhanced expression of pS484 as assessed by immunofluorescence or Western blotting. In platelets, pS484 rose rapidly and transiently upon stimulation. When a mutant form of kindlin-3, T482S484/AA kindlin-3, was transduced into mouse megakaryocytes, it failed to support activation of integrin αIIbβ3, whereas wild-type kindlin-3 did. In MDA-MB231 breast cancer cells, expression of T482S484/AA kindlin-3 suppressed cell spreading, migration, invasion, and VEGF production. Wild-type kindlin-3 expressing cells markedly increased tumor growth in vivo, whereas T482S484/AA kindlin-3 significantly blunted tumor progression. Thus, our data establish that a unique phosphorylation event in kindlin-3 regulates its cellular functions.

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FERMT3 contributes to glioblastoma cell proliferation and chemoresistance to temozolomide through integrin mediated Wnt signaling

Cited by 28 publications

References 39 publications

Identification of contributing genes of Huntington’s disease by machine learning

Identification of contributing genes of Huntington’s disease by machine learning

Wnt/β‐catenin signaling cascade: A promising target for glioma therapy

Site-specific phosphorylation regulates the functions of kindlin-3 in a variety of cells

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