RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Yao, Chengjun; Li, Panpan; Song, Hui; Song, Fuxi; Qu, Yalan; Ma, Xiaochen; Shi, Ranran; Wu, Jinsong

doi:10.1007/s12035-015-9340-x

Cited by 34 publications

(14 citation statements)

References 25 publications

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“…These reports agree well with our results. Other groups have also revealed the involvement of chemokine receptors in tumor EMT, such as CCR3 in colon cancer , CXCR4 in glioblastoma and CCR7 in pancreatic, gastric and ovarian carcinomas . Consistent with these reports, the current work again elucidates the pivotal role of chemokine receptors in cancer EMT, suggesting their value as promising therapeutic targets.…”

Section: Discussionsupporting

confidence: 86%

High expression of CCR5 in melanoma enhances epithelial–mesenchymal transition and metastasis via TGFβ1

Liu

Wang

et al. 2019

The Journal of Pathology

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Chemokine receptors are highly expressed in various cancers and play crucial roles in tumor progression. However, their expression patterns and functions in melanoma are unclear. The present study aimed to identify the chemokine receptors that play critical roles in melanoma progression and unravel the underlying molecular mechanisms. We found that CCR5 was more abundant in melanoma cells than normal cells and was positively associated with tumor malignancy in clinical patients. Animal experiments suggested that CCR5 deficiency in B16/F10 or A375 cells suppressed primary tumor growth and lung metastasis, whereas CCR5 overexpression in B16/F0 cells enhanced primary tumor growth and lung metastasis. CCR5 played a critical role in proliferation and migration of melanoma cells in vitro. Importantly, CCR5 was required for maintenance of the mesenchymal phenotype of metastatic melanoma cells. Mechanistically, CCR5 positively regulated expression of TGFβ1, which in turn induced epithelial–mesenchymal transition and migration via PI3K/AKT/GSK3β signaling. Collectively, our results establish a critical role of CCR5 expressed by melanoma cells in cancer progression and reveal the novel mechanisms controlling this process, which suggests the prognostic value of CCR5 in melanoma patients and provides novel insights into CCR5‐targeted strategies for melanoma treatment. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Section: Discussionsupporting

confidence: 86%

High expression of CCR5 in melanoma enhances epithelial–mesenchymal transition and metastasis via TGFβ1

Liu

Wang

et al. 2019

The Journal of Pathology

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“…Conversely, when we considered “incoming” signals to malignant cells, we found that CAFs expressed notably higher numbers of ligands that correspond to receptors expressed by the malignant cells of the corresponding tumor (hypergeometric test, p<0.05; Figures 4E and S5L). These included interactions that may promote EMT, such as TGFB3-TGFBR2, FGF7-FGFR2 and CXCL12-CXCR7 (Figure 4F) (Moustakas and Heldin, 2016; Ranieri et al, 2016; Yao et al, 2016). Accordingly, when we stained tumors for CAF markers (FAP, PDPN), we found that CAFs were present near p-EMT cells at the leading edge (Figures 4C and S5M).…”

Section: Resultsmentioning

confidence: 99%

Single-Cell Transcriptomic Analysis of Primary and Metastatic Tumor Ecosystems in Head and Neck Cancer

Puram

Tirosh

Parikh

et al. 2017

Cell

1,865

147

2,350

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SUMMARY The diverse malignant, stromal, and immune cells in tumors affect growth, metastasis and response to therapy. We profiled transcriptomes of ~6,000 single cells from 18 head and neck squamous cell carcinoma (HNSCC) patients, including five matched pairs of primary tumors and lymph node metastases. Stromal and immune cells had consistent expression programs across patients. Conversely, malignant cells varied within and between tumors in their expression of signatures related to cell cycle, stress, hypoxia, epithelial differentiation, and partial epithelial-to-mesenchymal transition (p-EMT). Cells expressing the p-EMT program spatially localized to the leading edge of primary tumors. By integrating single-cell transcriptomes with bulk expression profiles for hundreds of tumors, we refined HNSCC subtypes by their malignant and stromal composition, and established p-EMT as an independent predictor of nodal metastasis, grade, and adverse pathologic features. Our results provide insight into the HNSCC ecosystem and define stromal interactions and a p-EMT program associated with metastasis.

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“…Treatment with CXCL12 results in significant upregulation of Twist protein levels and promotion of EMT. In mice models, the activation of EMT creates an aggressive and invasive tumor phenotype [ 27 ].…”

Section: Opn Signaling and Transcriptional Regulation Of Emtmentioning

confidence: 99%

Osteopontin—A Master Regulator of Epithelial-Mesenchymal Transition

Kothari

Arffa

Chang

et al. 2016

JCM

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Osteopontin (OPN) plays an important functional role in both physiologic and pathologic states. OPN is implicated in the progression of fibrosis, cancer, and metastatic disease in several organ systems. The epithelial-mesenchymal transition (EMT), first described in embryology, is increasingly being recognized as a significant contributor to fibrotic phenotypes and tumor progression. Several well-established transcription factors regulate EMT and are conserved across tissue types and organ systems, including TWIST, zinc finger E-box-binding homeobox (ZEB), and SNAIL-family members. Recent literature points to an important relationship between OPN and EMT, implicating OPN as a key regulatory component of EMT programs. In this review, OPN’s interplay with traditional EMT activators, both directly and indirectly, will be discussed. Also, OPN’s ability to restructure the tissue and tumor microenvironment to indirectly modify EMT will be reviewed. Together, these diverse pathways demonstrate that OPN is able to modulate EMT and provide new targets for directing therapeutics.

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

Cited by 34 publications

References 25 publications

High expression of CCR5 in melanoma enhances epithelial–mesenchymal transition and metastasis via TGFβ1

High expression of CCR5 in melanoma enhances epithelial–mesenchymal transition and metastasis via TGFβ1

Single-Cell Transcriptomic Analysis of Primary and Metastatic Tumor Ecosystems in Head and Neck Cancer

Osteopontin—A Master Regulator of Epithelial-Mesenchymal Transition

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