Bone is the third most common site of cancer metastasis. Over 30 to 40% of lung cancers can develop skeletal metastasis and no effective curative therapy exists in clinic cases. Previously we screened the different expression of proteins between SBC-5 cells and SBC-3 cells by proteomic study methods (MALDI-TOF/TOF-MS) and found that calcineurin (hereafter referred as Cn) overexpresses in SBC-5 which has special priority in metastasis to bone in a multiple-organ metastasis mice model. However the roles of Cn in osteotropism of SCLC remain to be elucidated. At present study, we decrease CnAα expression in SBC-5 by lentiviral vector-mediated RNAi and found that down regulation of CnAα gene expression can decrease the proliferation and colony formation rate, impede the cell cycle progression, reduce the cell migration and invasion, and inhibit cells adhering to bone matrix, but not change the apoptosis rate of SBC-5 in vitro. In vivo down or up regulation of CnAα gene expression can only decrease or increase the bone metastasis rate, but not affect the metastasis rate to the visceral organs. Our research reveals that CnAα is closely related to the osteotropism metastasis of SCLC and a candidate tumor promotor gene for developing bone metastases.
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http://dx.doi.org/10.1007/s10585-011-9408-6 | DOI Listing |
Stem Cell Res Ther
January 2025
Shenzhen Key Laboratory of Epigenetics and Precision Medicine for Cancers, Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, 518116, China.
Background: Patient-derived lung cancer organoids (PD-LCOs) demonstrate exceptional potential in preclinical testing and serve as a promising model for the multimodal management of lung cancer. However, certain lung cancer cells derived from patients exhibit limited capacity to generate organoids due to inter-tumor or intra-tumor variability. To overcome this limitation, we have created an in vitro system that employs mesenchymal stromal cells (MSCs) or fibroblasts to serve as a supportive scaffold for lung cancer cells that do not form organoids.
View Article and Find Full Text PDFMol Ther
January 2025
San Raffaele Telethon Institute for Gene Therapy (SR-Tiget) IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita - Salute San Raffaele University Medical School, Milan, Italy; Pediatric Immunohematology and BMT, San Raffaele Hospital, Milan, Italy.
Hum Gene Ther
November 2024
Skeletal Dysplasia Research Lab, Nemours Children's Health, Wilmington, Delaware, USA.
Mucopolysaccharidosis IVA (MPS IVA) is an autosomal recessive disease caused by a mutation in the N-acetylgalactosamine-6-sulfate-sulfatase (GALNS) gene resulting in progressive systemic skeletal dysplasia. There is currently no effective treatment available for this skeletal condition. Thus, the development of a new therapy stands as an unmet challenge in reversing or alleviating the progression of the disease.
View Article and Find Full Text PDFNephrology (Carlton)
December 2024
Department of Endocrinology, the Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Background: Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta (PIK3CD) is the predominant isoform of the catalytic subunit of PI3K in lymphocytes. Based on comprehensive bioinformatics, this study explores the functions of PIK3CD in diabetic kidney disease (DKD) progression in mice and B lymphocyte activity.
Methods: Non-obese diabetic (NOD) mice that spontaneously develop DKD were applied as animal models.
Exp Ther Med
December 2024
Department of Spine Surgery, Ganzhou People's Hospital (The Affiliated Ganzhou Hospital of Jiangxi Medical College of Nanchang University, Ganzhou Hospital-Nanfang Hospital of Southern Medical University), Ganzhou, Jiangxi 341000, P.R. China.
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