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Molecular Biology in Bone Tumors

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 9535

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Prof. Dr. Chih-Hsin Tang

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Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
Interests: arthritis; bone cancer; osteoporosis; metastasis; drug development
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Dear Colleagues,

Bone tumors develop when cells within a bone divide uncontrollably, forming a lump or mass of abnormal tissue. Bone tumors can affect any bone in the body and develop in any part of the bone. A growing bone tumor destroys healthy tissue and weakens bone, making it more vulnerable to fracture. Primary bone cancers, including osteosarcoma, chondrosarcoma and Ewing’s sarcoma, begin in the bone. Secondary bone cancers, or bone metastases, begin somewhere else in the body (e.g., the breast, lung, prostate and thyroid) before metastasizing or spreading to bone. No cure exists for bone tumors. It is therefore crucial that we continue to research their pathogenesis and seek novel modes of therapy. We invite researchers to submit original research and review articles covering significant developments in the pathogenesis of bone tumors as well as novel medicines or strategies that hold promise in the prevention and/or treatment of this disease. In particular, we welcome research covering novel signaling pathways, signaling molecules, or discussions around bone tumor medications under development.

Prof. Dr. Chih-Hsin Tang
Guest Editor

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Keywords

osteosarcoma
chondrosarcoma
bone
tumor metastasis to bone
molecular mechanisms
treatment
prevention

Published Papers (4 papers)

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Research

14 pages, 2130 KiB

Open AccessArticle

MicroRNA-631 Resensitizes Doxorubicin-Resistant Chondrosarcoma Cells by Targeting Apelin

by Jui-Chieh Chen, Hsun-Chang Shih, Chih-Yang Lin, Jeng-Hung Guo, Cheng Huang, Hsiu-Chen Huang, Zhi-Yong Chong and Chih-Hsin Tang

Int. J. Mol. Sci. 2023, 24(1), 839; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24010839 - 03 Jan 2023

Cited by 4 | Viewed by 1636

Abstract

Chondrosarcoma is the second most common type of bone cancer. Surgical resection is the best choice for clinical treatment. High-grade chondrosarcoma is destructive and is more possible to metastasis, which is difficult to remove using surgery. Doxorubicin (Dox) is the most commonly used chemotherapy drug in the clinical setting; however, drug resistance is a major obstacle to effective treatment. In the present study, we compared Dox-resistant SW1353 cells to their parental cells using RNA sequencing (RNA-Seq). We found that the apelin (APLN) pathway was highly activated in resistant cells. In addition, tissue array analysis also showed that APLN was higher in high-grade tissues compared to low-grade tissues. APLN is a member of the adipokine family, which is a novel secreted peptide with multifunctional and biological activities. Previously, studies have shown that inhibition of the APLN axis may have a therapeutic benefit in cancers. However, the role of APLN in chondrosarcoma is completely unclear, and no related studies have been reported. During in vitro experiments, APLN was also observed to be highly expressed and secreted in Dox-resistant cells. Once APLN was knocked down, it could effectively improve its sensitivity to Dox. We also explored possible upstream regulatory microRNAs (miRNAs) of APLN through bioinformatics tools and the results disclosed that miR-631 was the most likely regulator of APLN. Furthermore, the expression of miR-631 was lower in the resistant cells, but overexpression of miR-631 in the Dox-resistant cell lines significantly increased the Dox sensitivity. These results were also observed in another chondrosarcoma cell line, JJ012 cells. Taken together, these findings will provide rationale for the development of drug resistance biomarkers and therapeutic strategies for APLN pathway inhibitors to improve the survival of patients with chondrosarcoma. Full article

(This article belongs to the Special Issue Molecular Biology in Bone Tumors)

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17 pages, 1822 KiB

Open AccessArticle

Integrated DNA Copy Number and Expression Profiling Identifies IGF1R as a Prognostic Biomarker in Pediatric Osteosarcoma

by Aaron M. Taylor, Jiayi M. Sun, Alexander Yu, Horatiu Voicu, Jianhe Shen, Donald A. Barkauskas, Timothy J. Triche, Julie M. Gastier-Foster, Tsz-Kwong Man and Ching C. Lau

Int. J. Mol. Sci. 2022, 23(14), 8036; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23148036 - 21 Jul 2022

Cited by 4 | Viewed by 2084

Abstract

Osteosarcoma is a primary malignant bone tumor arising from bone-forming mesenchymal cells in children and adolescents. Despite efforts to understand the biology of the disease and identify novel therapeutics, the survival of osteosarcoma patients remains dismal. We have concurrently profiled the copy number and gene expression of 226 osteosarcoma samples as part of the Strategic Partnering to Evaluate Cancer Signatures (SPECS) initiative. Our results demonstrate the heterogeneous landscape of osteosarcoma in younger populations by showing the presence of genome-wide copy number abnormalities occurring both recurrently among samples and in a high frequency. Insulin growth factor receptor 1 (IGF1R) is a receptor tyrosine kinase which binds IGF1 and IGF2 to activate downstream pathways involved in cell apoptosis and proliferation. We identify prevalent amplification of IGF1R corresponding with increased gene expression in patients with poor survival outcomes. Our results substantiate previously tenuously associated copy number abnormalities identified in smaller datasets (13q34+, 20p13+, 4q35-, 20q13.33-), and indicate the significance of high fibroblast growth factor receptor 2 (FGFR2) expression in distinguishing patients with poor prognosis. FGFR2 is involved in cellular proliferation processes such as division, growth and angiogenesis. In summary, our findings demonstrate the prognostic significance of several genes associated with osteosarcoma pathogenesis. Full article

(This article belongs to the Special Issue Molecular Biology in Bone Tumors)

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10 pages, 4062 KiB

Open AccessArticle

Diagnostic Utility of Genetic and Immunohistochemical H3-3A Mutation Analysis in Giant Cell Tumour of Bone

by Michał Wągrodzki, Andrzej Tysarowski, Katarzyna Seliga, Aneta Wojnowska, Maria Stepaniuk, Patrycja Castañeda Wysocka, Donata Makuła, Andrzej Pieńkowski, Bartłomiej Szostakowski, Renata Zub and Piotr Rutkowski

Int. J. Mol. Sci. 2022, 23(2), 969; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020969 - 16 Jan 2022

Cited by 7 | Viewed by 2406

Abstract

To validate the reliability and implementation of an objective diagnostic method for giant cell tumour of bone (GCTB). H3-3A gene mutation testing was performed using two different methods, Sanger sequencing and immunohistochemical (IHC) assays. A total of 214 patients, including 120 with GCTB and 94 with other giant cell-rich bone lesions, participated in the study. Sanger sequencing and IHC with anti-histone H3.3 G34W and G34V antibodies were performed on formalin-fixed, paraffin-embedded tissues, which were previously decalcified in EDTA if needed. The sensitivity and specificity of the molecular method was 100% (95% CI: 96.97–100%) and 100% (95% CI: 96.15–100%), respectively. The sensitivity and specificity of IHC was 94.32% (95% CI: 87.24–98.13%) and 100% (95% CI: 93.94–100.0%), respectively. P.G35 mutations were discovered in 2/9 (22.2%) secondary malignant GCTBs and 9/13 (69.2%) GCTB after denosumab treatment. We confirmed in a large series of patients that evaluation of H3-3A mutational status using direct sequencing is a reliable tool for diagnosing GCTB, and it should be incorporated into the diagnostic algorithm. Additionally, we discovered IHC can be used as a screening tool. Proper tissue processing and decalcification are necessary. The presence of the H3-3A mutation did not exclude malignant GCTB. Denosumab did not eradicate the neoplastic cell population of GCTB. Full article

(This article belongs to the Special Issue Molecular Biology in Bone Tumors)

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14 pages, 4046 KiB

Open AccessArticle

CCL4 Stimulates Cell Migration in Human Osteosarcoma via the mir-3927-3p/Integrin αvβ3 Axis

by Hsiao-Chi Tsai, Yan-You Lai, Hsuan-Chih Hsu, Yi-Chin Fong, Ming-Yu Lien and Chih-Hsin Tang

Int. J. Mol. Sci. 2021, 22(23), 12737; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222312737 - 25 Nov 2021

Cited by 11 | Viewed by 2681

Abstract

Osteosarcoma is the most common type of primary malignant bone cancer, and it is associated with high rates of pulmonary metastasis. Integrin αvβ3 is critical for osteosarcoma cell migratory and invasive abilities. Chemokine (C-C motif) ligand 4 (CCL4) has diverse effects on different cancer cells through its interaction with its specific receptor, C-C chemokine receptor type 5 (CCR5). Analysis of mRNA expression in human osteosarcoma tissue identified upregulated levels of CCL4, integrin αv and β3 expression. Similarly, an analysis of records from the Gene Expression Omnibus (GEO) dataset showed that CCL4 was upregulated in human osteosarcoma tissue. Importantly, the expression of both CCL4 and integrin αvβ3 correlated positively with osteosarcoma clinical stages and lung metastasis. Analysis of osteosarcoma cell lines identified that CCL4 promotes integrin αvβ3 expression and cell migration by activating the focal adhesion kinase (FAK), protein kinase B (AKT), and hypoxia inducible factor 1 subunit alpha (HIF-1α) signaling pathways, which can downregulate microRNA-3927-3p expression. Pharmacological inhibition of CCR5 by maraviroc (MVC) prevented increases in integrin αvβ3 expression and cell migration. This study is the first to implicate CCL4 as a potential target in the treatment of metastatic osteosarcoma. Full article

(This article belongs to the Special Issue Molecular Biology in Bone Tumors)

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