Material-induced Senescence (MIS): Fluidity Induces Senescent Type Cell Death of Lung Cancer Cells via Insulin-Like Growth Factor Binding Protein 5

Mano, Sharmy Saimon; Uto, Koichiro; Ebara, Mitsuhiro

doi:10.7150/thno.20582

Cited by 13 publications

(9 citation statements)

References 46 publications

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“…By binding to insulin-like growth factor (IGF), IGFBP5 plays an important role in cell differentiation and transcription (Amaar et al, 2002;Schedlich et al, 2007;Poreba and Durzynska, 2020). It can promote the proliferation and apoptosis of normal tissue cells and may further lead to tissue remodeling (Mano et al, 2017). Previous study discovered that IGFBP5 takes part in the progression of atherosclerosis (Xu et al, 2004;Yang et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Susceptibility Modules and Genes in Hypertrophic Cardiomyopathy by WGCNA and ceRNA Network Analysis

Sun

Xiao

Chen

et al. 2022

Front. Cell Dev. Biol.

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Background: We attempted to identify a regulatory competing endogenous RNA (ceRNA) network and a hub gene of Hypertrophic Cardiomyopathy (HCM).Methods: Microarray datasets of HCM tissue were obtained from NCBI Gene Expression Omnibus (GEO) database. The R package “limma” was used to identify differentially expressed genes. Online search databases were utilized to match the relation among differentially expressed long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and mRNAs. Weighted correlation network analysis (WGCNA) was used to identify the correlations between key modules and HCM. STRING database was applied to construct PPI networks. Gene Set Enrichment Analysis (GSEA) was used to perform functional annotations and verified the hub genes.Results: A total of 269 DE-lncRNAs, 63 DE-miRNAs and 879 DE-mRNAs were identified in myocardial tissues from microarray datasets GSE130036, GSE36946 and GSE36961, respectively. According to online databases, we found 1 upregulated miRNA hsa-miR-184 that was targeted by 2 downregulated lncRNAs (SNHG9, AC010980.2), potentially targeted 2 downregulated mRNAs (LRRC8A, SLC7A5). 3 downregulated miRNAs (hsa-miR-17-5p, hsa-miR-876-3p, hsa-miR-139-5p) that were targeted by 9 upregulated lncRNAs, potentially targeted 21 upregulated mRNAs. Black and blue modules significantly related to HCM were identified by WGCNA. Hub gene IGFBP5 regulated by hsa-miR-17-5p, AC007389.5, AC104667.1, and AC002511.2 was identified. GSEA indicated that IGFBP5 might involve in the synthesis of myosin complex, participate in kinesin binding, motor activity and function via the regulation of actin cytoskeleton.Conclusion: The results provide a potential molecular regulatory mechanism for the diagnosis and treatment of HCM. IGFBP5 might play an important role in the progression of HCM.

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Section: Discussionmentioning

confidence: 99%

Susceptibility Modules and Genes in Hypertrophic Cardiomyopathy by WGCNA and ceRNA Network Analysis

Sun

Xiao

Chen

et al. 2022

Front. Cell Dev. Biol.

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“…In our previous report, we showed that the material fluidity induces senescent type cell death in cancer cells which halt cancer metastasis [16]. In this study, we propose that the material fluidity or viscosity induce EMT in MCF-7 cells.…”

Section: Introductionmentioning

confidence: 51%

Fluidity of Poly (ε-Caprolactone)-Based Material Induces Epithelial-to-Mesenchymal Transition

Mano

Uto

Ebara

2020

IJMS

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Background: We propose the potential studies on material fluidity to induce epithelial to mesenchymal transition (EMT) in MCF-7 cells. In this study, we examined for the first time the effect of material fluidity on EMT using poly(ε-caprolactone-co-D,L-lactide) (P(CL-co-DLLA)) with tunable elasticity and fluidity. Methods: The fluidity was altered by chemically crosslinking the polymer networks. The crosslinked P(CL-co-DLLA) substrate showed a solid-like property with a stiffness of 261 kPa, while the non-crosslinked P(CL-co-DLLA) substrate of 100 units (high fluidity) and 500 units (low fluidity) existed in a quasi-liquid state with loss modulus of 33 kPa and 30.8 kPa, respectively, and storage modulus of 10.8 kPa and 20.1 kPa, respectively. Results: We observed that MCF-7 cells on low fluidic substrates decreased the expression of E-cadherin, an epithelial marker, and increased expression of vimentin, a mesenchymal marker. This showed that the cells lose their epithelial phenotype and gain a mesenchymal property. On the other hand, MCF-7 cells on high fluidic substrates maintained their epithelial phenotype, suggesting that the cells did not undergo EMT. Conclusion: Considering these results as the fundamental information for material fluidity induced EMT, our system could be used to regulate the degree of EMT by turning the fluidity of the material.

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“…Increased IGF function may promote cell mitosis, thereby accelerating cell proliferation and promoting tumor growth (30–32). Studies have demonstrated that IGF is closely associated with lung cancer progression (33,34). Thus, the inhibition of ACAT-1 expression reduces cholesterol ester levels, and may thereby result in decreased IGF activity, resulting in the inactivation of phosphoinositide 3 kinase/protein kinase B or RAS type GTPase family/mitogen-activated protein kinase signaling pathways, thereby inhibiting tumor growth and metastasis (35).…”

Section: Discussionmentioning

confidence: 99%

Effect of inhibiting ACAT‑1 expression on the growth and metastasis of Lewis lung carcinoma

Qiao

Zhang

et al. 2019

Oncol Lett

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Accumulating evidence suggests that acetyl-CoA acetryltransferase 1 (ACAT-1) may mediate tumor development and metastasis. However, the specific function served by ACAT-1 in lung cancer is not well understood. Therefore, the present study initially verified that ACAT-1 was overexpressed in Lewis lung carcinoma (LLC) tissues compared with non-LLC mice and that this overexpression promoted the proliferation, invasion and metastasis of these LLC samples. Western blotting, immunofluorescence microscopy and flow cytometry allowed the present study to determine that the ACAT-1 inhibitor avasimibe significantly reduced the expression of ACAT-1 in LLC compared with LLC cells that are not treated with avasimibe (P<0.05). A combination of Cell Counting Kit-8 and wound healing assays demonstrated that downregulating ACAT-1 expression sufficiently inhibited the proliferation of LLC cells. Avasimibe promoted LLC cell apoptosis as assessed by a Annexin V/propidium iodide double staining assay. Furthermore, avasimibe inhibited tumor growth in vivo and improved immune responses, with tissue biopsies from LLC model mice exhibiting higher levels of ACAT-1 compared with in healthy controls. Altogether, the results of the present study reveal that avasimibe may inhibit the progression of LLC by downregulating the expression of ACAT-1, which may thus be a potential novel therapeutic target for lung cancer treatment.

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Material-induced Senescence (MIS): Fluidity Induces Senescent Type Cell Death of Lung Cancer Cells via Insulin-Like Growth Factor Binding Protein 5

Cited by 13 publications

References 46 publications

Susceptibility Modules and Genes in Hypertrophic Cardiomyopathy by WGCNA and ceRNA Network Analysis

Susceptibility Modules and Genes in Hypertrophic Cardiomyopathy by WGCNA and ceRNA Network Analysis

Fluidity of Poly (ε-Caprolactone)-Based Material Induces Epithelial-to-Mesenchymal Transition

Effect of inhibiting ACAT‑1 expression on the growth and metastasis of Lewis lung carcinoma

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