Natural Diterpenoid Isoferritin A (IsoA) Inhibits Glioma Cell Growth and Metastasis via Regulating of TGFβ-Induced EMT Signal Pathway

Shen, Bin; Sun, Dezhou

doi:10.12659/msm.910102

Cited by 7 publications

(5 citation statements)

References 27 publications

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“…EMT is associated with aberrant expression levels of related cytokines and transcription factors; for example, the epithelial phenotype marker E-cadherin is downregulated and the mesenchymal phenotype markers vimentin and N-cadherin are upregulated during EMT ( Fischer et al, 2015 ). As an epithelial biomarker, E-cadherin has been proven to play an important role in tumor metastasis ( Rötzer et al, 2015 ; Shen and Sun, 2018 ; Wu et al, 2018 ). Studies have found that CHIP functions as an oncogene by inhibiting E-cadherin ( Xu et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Multi-Omics Analysis of the Therapeutic Value of MAL2 Based on Data Mining in Human Cancers

Yuan

Jiang

Lan

et al. 2022

Front. Cell Dev. Biol.

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Recent studies have reported that T-cell differentiation protein 2 (MAL2) is an important regulator in cancers. Here, we downloaded data from multiple databases to analyze MAL2 expression and function in pan-cancers, especially in ovarian cancer (OC). Gene Expression Profiling Interactive Analysis (GEPIA) databases was used to examine MAL2 expression in 13 types of cancer. Kaplan–Meier plotter database was used to analyze the overall survival rate of MAL2 in pan-cancers. The Catalog of Somatic Mutations in Cancer (COSMIC), cBioPortal, and UCSC databases were used to examine MAL2 mutation in human cancers. Metascape, STRING, and GeneMANIA websites were used to explore MAL2 function in OC. Furthermore, ggplot2 package and ROC package were performed to analyze hub gene expression and undertake receiver operating characteristic (ROC) analysis. Drug sensitivity of MAL2 in OC was examined by the GSCALite database. In order to verify the results from databases above, real-time quantitative polymerase chain reaction (qRT-PCR) and western blotting were conducted to detect the expression of MAL2 in OC cells. CRISPR/Cas9 system was used to knockout the MAL2 gene in the OC cell lines HO8910 and OVCAR3, using specific guide RNA targeting the exons of MAL2. Then, we performed proliferation, colony formation, migration, and invasion assays to investigate the impact of MAL2 in OC cell lines in vivo and in vitro. Epithelial-mesenchymal transition (EMT)-associated biomarkers were significantly altered in vitro via western blotting and qRT-PCR. Taken together, we observed that MAL2 was remarkably dysregulated in multiple cancers and was related to patient overall survival (OS), mutation, and drug sensitivity. Furthermore, experimental results showed that MAL2 deletion negatively regulated the proliferation, migration, invasion, and EMT of OC, indicating that MAL2 is a novel oncogene that can activate EMT, significantly promote both the proliferation and migration of OC in vitro and in vivo, and provide new clues for treatment strategies.

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Section: Discussionmentioning

confidence: 99%

Multi-Omics Analysis of the Therapeutic Value of MAL2 Based on Data Mining in Human Cancers

Yuan

Jiang

Lan

et al. 2022

Front. Cell Dev. Biol.

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“…2B). EC occurrence is a complex process, including vascular production, cell adhesion, motility, Extracellular Matrix (ECM) degradation and angiogenesis [18][19][20][21][22] . EC patients diagnosed at an advanced stage usually have a poor prognosis [6] .…”

Section: Resultsmentioning

confidence: 99%

Overexpression of C1QTNF6 in Esophageal Cancer and Promotes the Proliferation and Migration of Esophageal Cancer Cells

Xia¹,

Lu²,

Yu³

et al. 2022

IJPS

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Esophageal cancer is a common cancer among people in the world. The molecular mechanism of complement C1q tumor necrosis factor related protein 6 in esophageal cancer is still unclear. This article aimed to clarify the role of complement C1q tumor necrosis factor related protein 6 in esophageal cancer. The expression of complement C1q tumor necrosis factor related protein 6 in esophageal cancer tissues was detected using quantitative real-time polymerase chain reaction and Western blot. Furthermore, short hairpin ribonucleic acid was used to knockdown the expression of complement C1q tumor necrosis factor related protein 6 in esophageal cancer cell lines. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide, wound healing assays and transwell assays were used to determine the role of complement C1q tumor necrosis factor related protein 6 in esophageal cancer cells. In our research, we found that the expression of complement C1q tumor necrosis factor related protein 6 was up-regulated in esophageal cancer tissues. The increased expression of complement C1q tumor necrosis factor related protein 6 was significantly correlated with tumor stage and lymph node metastasis. The proliferation and migration of esophageal cancer cells were inhibited after complement C1q tumor necrosis factor related protein 6-short hairpin ribonucleic acid transfection in vitro. These results suggested that complement C1q tumor necrosis factor related protein 6 serves as an oncogene and promotes cell proliferation and migration in esophageal cancer. In addition, complement C1q tumor necrosis factor related protein 6 may be a potential therapeutic target for esophageal cancer patients.

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“…The TGF- β exerts its regulatory effects on GBM by controlling the activation of the EMT with both Smad-independent and Smad-dependent patterns, finally resulting in poor prognoses [ 32 ]. Previous studies have described enhancement of the E/N-cadherin transition, vimentin, and neurocadherin expressions, as well as attenuation of epithelial calmodulin expressions by TGF- β [ 33 ]. TGF- β combines with the receptors TGF- β RI/II to activate various downstream signaling pathways, including Smad, MAPK, and PI3K/Akt.…”

Section: Discussionmentioning

confidence: 99%

HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma

Sun

Zheng

Cai

et al. 2022

Journal of Oncology

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Background. The HOX gene family of transcription factors, characterized by conserved homeodomains, is positively correlated with the resistance to chemotherapy drugs and poor prognosis, as well as the initiating potential of gliomas. However, there are few studies regarding the HOXC6 gene in glioma cells. Therefore, in the present study, we explored the regulatory roles and detailed mechanisms underlying the relationship between HOXC6 and the progression of GBM. Methods. The expression levels and prognostic value of HOXC6 in GBM were evaluated using the data obtained from the GCCA, GEPIA, and ONCOMINE databases. The relationship between GBM prognosis and levels of HOXC6 was identified using Kaplan-Meier curves. The protein levels of HOXC6 in GBM and adjacent normal tissues were identified via Western blot and immunohistochemistry (IHC) staining methods. Lentiviruses containing full-length HOXC6 and HOXC6 specific siRNA sequences were used to overexpress and knock down, respectively, the expression of HOXC6 in U87 and U251 cells. The role of HOXC6 in the regulation of migration and proliferation of GBM cells was accessed using Transwell, wound healing, CCK-8, and colony formation assays. The activation of the TGF-β/Smad signaling pathway was detected via Western blotting. Results. Compared to normal tissues and control cells, GBM tissues and cell lines showed higher expressions of HOXC6. The expression of HOXC6 was associated with disease-free and the overall survival of GBM patients. Additionally, positive correlations between the expression of HOXC6 and the migration and proliferation of GBM cells were observed in vitro. The mechanistic analyses indicated that HOXC6 exerts its promotive effect on the progression and invasion of glioma cells by promoting the activation of the EMT and TGF-β/Smad signaling pathways. Conclusions. HOXC6 enhances the migration and proliferation of GBM by activating the EMT signaling pathway.

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Natural Diterpenoid Isoferritin A (IsoA) Inhibits Glioma Cell Growth and Metastasis via Regulating of TGFβ-Induced EMT Signal Pathway

Cited by 7 publications

References 27 publications

Multi-Omics Analysis of the Therapeutic Value of MAL2 Based on Data Mining in Human Cancers

Multi-Omics Analysis of the Therapeutic Value of MAL2 Based on Data Mining in Human Cancers

Overexpression of C1QTNF6 in Esophageal Cancer and Promotes the Proliferation and Migration of Esophageal Cancer Cells

HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma

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