Collagen triple helix repeat containing 1 (CTHRC1), an extracellular matrix-related protein, has been found to be upregulated in many solid tumors and contributes to tumorigenesis. We found that CTHRC1 is overexpressed in glioblastoma tissues and cells. By using the technique of RNA interference, the expression of CTHRC1 in the human glioblastoma U-87MG cell line was downregulated, and the proliferation and migration of U-87MG cells were examined. The results showed that the knockdown of CTHRC1 exerts inhibitory effects on the proliferation and migration ability of U-87MG cells. Knockdown of CTHRC1 expression in U-87MG cells resulted in upregulation in the expression of E-cadherin and downregulation in the expression of N-cadherin, SNAIL, and Slug, suggesting that CTHRC1 inhibits glioblastoma cell migration by suppressing epithelial-mesenchymal transition (EMT). Knockdown of CTHRC1 led to remarkably decreased β-catenin protein levels in the nucleus. These results indicate that CTHRC1 might play an important role in the development of glioblastoma and offer a candidate molecular target for glioblastoma prevention and therapy.

Knockdown of Collagen Triple Helix Repeat Containing 1 (CTHRC1) Inhibits Epithelial-Mesenchymal Transition and Cellular Migration in Glioblastoma Cells.

The focus of radiation biodosimetry has changed recently, and a paradigm shift for using molecular technologies of omic platforms in addition to cytogenetic techniques has been observed. In our study, we have used a nonhuman primate model to investigate the impact of a supralethal dose of 12 Gy radiation on alterations in the lung transcriptome. We used 6 healthy and 32 irradiated animal samples to delineate radiation-induced changes. We also used a medical countermeasure, γ-tocotrienol (GT3), to observe any changes. We demonstrate significant radiation-induced changes in the lung transcriptome for total-body irradiation (TBI) and partial-body irradiation (PBI). However, no major influence of GT3 on radiation was noted in either comparison. Several common signaling pathways, including PI3K/AKT, GADD45, and p53, were upregulated in both exposures. TBI activated DNA-damage-related pathways in the lungs, whereas PTEN signaling was activated after PBI. Our study highlights the various transcriptional profiles associated with γ- and X-ray exposures, and the associated pathways include LXR/RXR activation in TBI, whereas pulmonary wound-healing and pulmonary fibrosis signaling was repressed in PBI. Our study provides important insights into the molecular pathways associated with irradiation that can be further investigated for biomarker discovery. 

Lung transcriptome of nonhuman primates exposed to total- and partial-body irradiation

High-grade osteosarcomas are the most frequent malignant bone tumors in the pediatric population, with 150 patients diagnosed every year in France. Osteosarcomas are associated with low survival rates for high risk patients (metastatic and relapsed diseases). Knowing that the canonical Wnt signaling pathway (Wnt/β-catenin) plays a complex but a key role in primary and metastatic development of osteosarcoma, the aim of this work was to analyze the effects of ICG-001, a CBP/β-catenin inhibitor blocking the β-catenin dependent gene transcription, in three human osteosarcoma cell lines (KHOS, MG63 and 143B). The cell proliferation and migration were first evaluated in vitro after ICG-001 treatment. Secondly, a mouse model of osteosarcoma was used to establish the in vivo biological effect of ICG-001 on osteosarcoma growth and metastatic dissemination. In vitro, ICG-001 treatment strongly inhibits osteosarcoma cell proliferation through a cell cycle blockade in the G0/G1 phase, but surprisingly, increases cell migration of the three cell lines. Moreover, ICG-001 does not modulate tumor growth in the osteosarcoma mouse model but, rather significantly increases the metastatic dissemination to lungs. Taken together, these results highlight, despite an anti-proliferative effect, a deleterious pro-migratory role of ICG-001 in osteosarcoma.

https://www.mdpi.com/1424-8247/14/5/421/pdf

ICG-001, an Inhibitor of the β-Catenin and cAMP Response Element-Binding Protein Dependent Gene Transcription, Decreases Proliferation but Enhances Migration of Osteosarcoma Cells.

Oral squamous cell carcinoma (OSCC) is a common type of malignant oral cancer that has a high recurrence rate. Voltage-gated sodium channel Nav1.5 was reported to be highly up-regulated in various types of cancers. However, the regulatory mechanism of Nav1.5 in cancers including OSCC still remains elusive. In this study, Nav1.5 was found to be highly expressed in OSCC tissues and cells. Through the analysis of clinical characteristics of patients, we found that the expression level of Nav1.5 was closely related to neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, tumor-node-metastasis stage, and lymph node metastasis. Moreover, we found that Nav1.5 mainly located on the cell membrane as well as cytoplasm and knockdown of Nav1.5 promoted cell apoptosis and decreased proliferation in OSCC. Transwell assay results showed that knockdown of Nav1.5 effectively suppressed the migration and invasion in OSCC. In addition, knockdown of Nav1.5 was found to inhibit the protein and mRNA expression levels of β-catenin, cyclin D1, and c-Myc in the Wnt/β-catenin signaling pathway. In summary, these results indicated that Nav1.5 may be involved in the progression of OSCC through the Wnt/β-catenin signaling pathway.

Knockdown of Nav1.5 inhibits cell proliferation, migration and invasion via Wnt/β-catenin signaling pathway in oral squamous cell carcinoma.

Ionizing radiation (IR) has been shown to play a crucial role in the treatment of glioblastoma (GBM; grade IV) and non-small-cell lung cancer (NSCLC). Nevertheless, recent studies have indicated that radiotherapy can offer only palliation owing to the radioresistance of GBM and NSCLC. Therefore, delineating the major radioresistance mechanisms may provide novel therapeutic approaches to sensitize these diseases to IR and improve patient outcomes. This review provides insights into the molecular and cellular mechanisms underlying GBM and NSCLC radioresistance, where it sheds light on the role played by cancer stem cells (CSCs), as well as discusses comprehensively how the cellular dormancy/non-proliferating state and polyploidy impact on their survival and relapse post-IR exposure.

/pdf/the-molecular-and-cellular-strategies-of-glioblastoma-and-1ckd0q4n.pdf

The Molecular and Cellular Strategies of Glioblastoma and Non-Small-Cell Lung Cancer Cells Conferring Radioresistance

Thyroid cancer 1 (TC-1, C8ofr4) is widely expressed in vertebrates and associated with many kinds of tumors. Previous studies indicated that TC-1 functions as a positive regulator in the Wnt/β-catenin signaling pathway in non-small cell lung cancer (NSCLC). However, its exact role and regulation mechanism in radiosensitivity of NSCLC are still unclear. The expression level of TC-1 was measured by qRT-PCR and western blot in NSCLC cell lines. Proliferation and apoptosis of NSCLC cells in response to TC-1 knockdown or/and radiation were determined by MTT assay and flow cytometry, respectively. The activation of the Wnt/β-catenin signaling pathway was further examined by western blotin vitroandin vivo Compared to TC-1 siRNA or radiotherapy alone, TC-1 silencing combined with radiation inhibited cell proliferation and induced apoptosis in NSCLC cell lines by inactivating of the Wnt/β-catenin signaling pathway. Furthermore, inhibition of the Wnt/β-catenin signaling pathway by XAV939, a Wnt/β-catenin signaling inhibitor, contributed to proliferation inhibition and apoptosis induction in NSCLC A549 cells. Combinative treatment of A549 xenografts with TC-1 siRNA and radiation caused significant tumor regression and inactivation of the Wnt/β-catenin signaling pathway relative to TC-1 siRNA or radiotherapy alone. The results fromin vitroandin vivostudies indicated that TC-1 silencing sensitized NSCLC cell lines to radiotherapy through the Wnt/β-catenin signaling pathway.

Knockdown of TC-1 enhances radiosensitivity of non-small cell lung cancer via the Wnt/β-catenin pathway

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Knockdown of TC-1 enhances radiosensitivity of non-small cell lung cancer via the Wnt/β-catenin pathway