Ikaros inhibits proliferation and, through upregulation of Slug, increases metastatic ability of ovarian serous adenocarcinoma cells

He, Li Cai; Gao, Feng; Xu, Han; Zhao, Shan; Min, Chun; Li, June; Zhang, Shu; Wu, Ying

doi:10.3892/or.2012.1946

Cited by 22 publications

(17 citation statements)

References 32 publications

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“…Tumor growth was observed for at least cycle and wound healing assay, functional studies demonstrated that the Twist pathway indeed affected CXCL12-mediated proliferation, migration, and invasion of glioblastoma cells. Consistent with these findings, published articles also laid stress on the regulatory functions of Twist in cell migration and invasion [24,25]. Twist indeed plays different roles in tumor development.…”

Section: Discussionsupporting

confidence: 63%

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Yao

Song

et al. 2015

Mol Neurobiol

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In recent decades, the chemokine receptor CXCR4 and its ligand CXCL12 have been extensively reported to be associated with tumorigenesis. In addition, Twist signaling induces the epithelial-mesenchymal transition (EMT) process in glioblastoma development. In the present study, in vitro assays were used to investigate the role of CXCR4 and Twist in human glioblastoma. We explored the impact of CXCR4 and Twist on human glioblastoma using in vitro protein and gene assays. We found the administration of CXCL12 upregulated the expression of p-ERK, p-AKT, Twist, N-cadherin, and MMP9 in U87 cells, whereas the increase of E-cadherin protein was affected. Subsequently, Twist activity and EMT signaling were directly influenced by PD98059 and LY294002. Most importantly, the genetic silencing of Twist inhibited CXCL12-induced EMT occurrence, including proliferation, migration, and tumor formation of U87 cells. In conclusion, CXCL12/CXCR4 pathway activates ERK and PI3K/AKT signaling to upregulate Twist pathway, leading to the progression of EMT in human glioblastoma. Our study creates a new stage for molecule-targeted therapy of human glioblastoma.

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Section: Discussionsupporting

confidence: 63%

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Yao

Song

et al. 2015

Mol Neurobiol

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“…However, the role of Ikaros family members in solid tumors have not been well demonstrated in the literature. IKZF1 promotes metastatic ability through upregulating Slug and matrix metalloproteinase 2 (MMP2) in ovarian cancer 30 . Li et al .…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Aiolos promotes epithelial-mesenchymal transition and cancer stem cell-like properties in lung cancer cells

Hung

Kao

Huang³

et al. 2019

Sci Rep

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Aiolos/Ikaros family zinc finger 3 (IKZF3), a member of the Ikaros family of lymphocyte maturation-driving transcription factors, is highly expressed in hematopoietic malignancies. However, its role in epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC)-like properties in lung cancer remains unknown. Human lung cancer cell lines H1299 with overexpressing Aiolos (H1299-Aiolos) and A549 with overexpressing Aiolos (A549-Aiolos) were generated by stable transfection. Cell migration and invasion assays were done to demonstrate their invasion and migration ability. Sphere formation assay was used to determine their tumor-initiating capability. Aiolos overexpression induced EMT and increased migration/invasiveness in H1299 and A549 cells. Aiolos overexpression also increased metastatic ability in vivo . Aiolos overexpression upregulated the expression of Twist and matrix metalloproteinase 16 (MMP16). By using knockdown of Twist or an inhibitor of phosphatidylinositol (PI) 3-kinase, EMT, migration/invasiveness ability, and MMP16 expression were reversed in H1299-Aiolos and A549-Aiolos cells. Overexpression of Aiolos upregulated the CSC-like properties in lung cancer cells, and were also reversed by an inhibitor of PI 3-kinase. For lung cancer cells, Aiolos overexpression promotes EMT and CSC-like properties through upregulating the PI 3-kinase/Akt pathway. The information is helpful for developing therapeutic strategies targeting Aiolos expression for lung cancer treatment.

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“…Emerging evidence demonstrated that dysregulation of expression of miRNAs in gastric cancer might be thought as one of the leading factors in tumorigenesis, and miRNAs can be recommended as a predictive biomarker in the diagnosis of gastric cancer patients. Besides, Twist1 has been widely reported as a poor prognosis biomarker in diverse tumors [17–19]. Thus, identification of GC-related miRNAs will make for understanding of etiology of gastric cancer, and elucidation of their biological roles can facilitate the diagnosis and prognosis of gastric cancer patients.…”

Section: Discussionmentioning

confidence: 99%

miR-186 affects the proliferation, invasion and migration of human gastric cancer by inhibition of Twist1

et al. 2016

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Recent evidence shows that miRNAs are dysregulated in a variety of cancers including gastric cancer (GC), and emerging as key oncogenes or tumor suppressors. In this study, qRT-PCR was used to analyze the expression of miR-186 in GC tissues and adjacent non-cancerous tissues, and then more in-vitro experiments were used to investigate the role of miR-186 in GC cells. Here, we identified miR-186 was generally down-regulated in GC tissues; however, Twist1 was generally up-regulated in GC tissues. Moreover, miR-186 and Twist1 were associated with larger tumor size and advanced clinical stage of GC. In-vitro experiments demonstrated that ectopic overexpression of miR-186 inhibited GC cell proliferation, invasion and migration; however, inhibited expression of miR-186 enhanced cell proliferation, invasion and migration. Furthermore, the luciferase reporter assay demonstrated Twist1 as a direct target of miR-186. Finally, over-expression of Twist1 abrogated inhibitory impact of miR-186 on cell proliferation, invasion and migration. In conclusion, miR-186 affects the proliferation, invasion and migration of human gastric cancer by inhibition of Twist1, and could be a tumor suppressor in GC development. Thus, miR-186 may be served as a candidate prognostic biomarker and target for new therapies in human gastric cancer.

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Ikaros inhibits proliferation and, through upregulation of Slug, increases metastatic ability of ovarian serous adenocarcinoma cells

Cited by 22 publications

References 32 publications

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Overexpression of Aiolos promotes epithelial-mesenchymal transition and cancer stem cell-like properties in lung cancer cells

miR-186 affects the proliferation, invasion and migration of human gastric cancer by inhibition of Twist1

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