&lt;p&gt;MiR-145 inhibits EGF-induced epithelial-to-mesenchymal transition via targeting Smad2 in human glioblastoma&lt;/p&gt;

Chen, Weijie; Huang, Baochen; Wang, Enqin; Wang, Xingqiang

doi:10.2147/ott.s202129

Cited by 8 publications

(5 citation statements)

References 24 publications

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“…In recent studies, miR-145 has been proven to inhibit the proliferation, invasion, and metastasis of tumor cells; increase the sensitivity of tumor cells to chemotherapy; and regulate the occurrence and development of tumors by targeting ADAM17 in several malignant tumors [23,[37][38][39][40]. In particular, several studies have indicated that miR-145 could inhibit epithelial-to-mesenchymal transition [41], migration, and invasion [23] and increase the cytotoxicity of drug treatment in GBM [42,43]. Furthermore, the potential of miR-145 as a biomarker for predicting clinical outcomes of patients with GBM has been demonstrated [44,45].…”

Section: Discussionmentioning

confidence: 99%

ADAM17 Confers Temozolomide Resistance in Human Glioblastoma Cells and miR-145 Regulates Its Expression

Yang

Lee

Huang

et al. 2023

IJMS

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Glioblastoma (GBM) is a malignant brain tumor, commonly treated with temozolomide (TMZ). Upregulation of A disintegrin and metalloproteinases (ADAMs) is correlated to malignancy; however, whether ADAMs modulate TMZ sensitivity in GBM cells remains unclear. To explore the role of ADAMs in TMZ resistance, we analyzed changes in ADAM expression following TMZ treatment using RNA sequencing and noted that ADAM17 was markedly upregulated. Hence, we established TMZ-resistant cell lines to elucidate the role of ADAM17. Furthermore, we evaluated the impact of ADAM17 knockdown on TMZ sensitivity in vitro and in vivo. Moreover, we predicted microRNAs upstream of ADAM17 and transfected miRNA mimics into cells to verify their effects on TMZ sensitivity. Additionally, the clinical significance of ADAM17 and miRNAs in GBM was analyzed. ADAM17 was upregulated in GBM cells under serum starvation and TMZ treatment and was overexpressed in TMZ-resistant cells. In in vitro and in vivo models, ADAM17 knockdown conferred greater TMZ sensitivity. miR-145 overexpression suppressed ADAM17 and sensitized cells to TMZ. ADAM17 upregulation and miR-145 downregulation in clinical specimens are associated with disease progression and poor prognosis. Thus, miR-145 enhances TMZ sensitivity by inhibiting ADAM17. These findings offer insights into the development of therapeutic approaches to overcome TMZ resistance.

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Section: Discussionmentioning

confidence: 99%

ADAM17 Confers Temozolomide Resistance in Human Glioblastoma Cells and miR-145 Regulates Its Expression

Yang

Lee

Huang

et al. 2023

IJMS

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“…Some miRNAs modulate the expression of genes, such as E-CADHERIN, MMP9, MMP14, SLUG, MMP2, and SNAIL, that are associated with GBM invasion and PMT 118 . In contrast, miRNAs can inhibit MT by directly targeting and inhibiting the expression of factors such as the FZD6 and FZD7 receptors 119,120 ; the transcription inhibitors ZEB1 and ZEB2 121,122 ; proteins such as Smad2, LHFPL3, and ADAM19 [123][124][125] ; and factors associated with TGF-β 126,127 and NF-κB 128,129 pathways. Furthermore, some miRNAs are involved in cell-to-cell communication and intercellular interactions mediating MT in GBM 130 .…”

Section: Micrornas (Mirnas)mentioning

confidence: 99%

Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition

Xu,

Hou,

et al. 2024

Cancer Biol Med

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Among central nervous system-associated malignancies, glioblastoma (GBM) is the most common and has the highest mortality rate. The high heterogeneity of GBM cell types and the complex tumor microenvironment frequently lead to tumor recurrence and sudden relapse in patients treated with temozolomide. In precision medicine, research on GBM treatment is increasingly focusing on molecular subtyping to precisely characterize the cellular and molecular heterogeneity, as well as the refractory nature of GBM toward therapy. Deep understanding of the different molecular expression patterns of GBM subtypes is critical. Researchers have recently proposed tetra fractional or tripartite methods for detecting GBM molecular subtypes. The various molecular subtypes of GBM show significant differences in gene expression patterns and biological behaviors. These subtypes also exhibit high plasticity in their regulatory pathways, oncogene expression, tumor microenvironment alterations, and differential responses to standard therapy. Herein, we summarize the current molecular typing scheme of GBM and the major molecular/genetic characteristics of each subtype. Furthermore, we review the mesenchymal transition mechanisms of GBM under various regulators.

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“…It is known to all that epidermal growth factor (EGF) can induce the EMT process by repressing the expression of Ecadherin, the main epithelial marker and up-regulating mesothelial markers vimentin and N-cadherin (147). Gonzaĺez-Gonzaĺez L. et al reported that EGF stimulated the migratory capacity of breast cancer cells, by regulating the functional expression of NaV1.5 channels.…”

Section: Non-digestive Cancersmentioning

confidence: 99%

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

et al. 2021

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Epithelial-to-mesenchymal transition (EMT), a complicated program through which polarized epithelial cells acquire motile mesothelial traits, is regulated by tumor microenvironment. EMT is involved in tumor progression, invasion and metastasis via reconstructing the cytoskeleton and degrading the tumor basement membrane. Accumulating evidence shows that resveratrol, as a non-flavonoid polyphenol, can reverse EMT and inhibit invasion and migration of human tumors via diverse mechanisms and signaling pathways. In the present review, we will summarize the detailed mechanisms and pathways by which resveratrol and its analogs (e.g. Triacetyl resveratrol, 3,5,4’-Trimethoxystilbene) might regulate the EMT process in cancer cells to better understand their potential as novel anti-tumor agents. Resveratrol can also reverse chemoresistance via EMT inhibition and improvement of the antiproliferative effects of conventional treatments. Therefore, resveratrol and its analogs have the potential to become novel adjunctive agents to inhibit cancer metastasis, which might be partly related to their blocking of the EMT process.

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<p>MiR-145 inhibits EGF-induced epithelial-to-mesenchymal transition via targeting Smad2 in human glioblastoma</p>

Cited by 8 publications

References 24 publications

ADAM17 Confers Temozolomide Resistance in Human Glioblastoma Cells and miR-145 Regulates Its Expression

ADAM17 Confers Temozolomide Resistance in Human Glioblastoma Cells and miR-145 Regulates Its Expression

Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

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