The efficacy and safety comparison of first-line chemotherapeutic agents (high-dose methotrexate, doxorubicin, cisplatin, and ifosfamide) for osteosarcoma: a network meta-analysis

Zhang, Bin; Zhang, Yan; Li, Rongzhen; Li, Jiazhen; Lu, Xin; Zhang, Yi

doi:10.1186/s13018-020-1576-0

Cited by 64 publications

(52 citation statements)

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“…Although they represent the main available treatment in osteosarcoma, chemotherapeutics are also toxic to normal tissue, and can lead to myelosuppression, opportunistic infection, heart damage and other adverse reactions, thereby decreasing the patient survival rate and quality of life ( 17 ). Therefore, new agents with fewer side effects and improved therapeutic advantages are required.…”

Section: Discussionmentioning

confidence: 99%

Punicalagin inhibited proliferation, invasion and angiogenesis of osteosarcoma through suppression of NF‑κB signaling

2020

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Osteosarcoma is the most common primary malignant bone tumor among children and young people and is associated with poor prognosis. Punicalagin is an antioxidant ellagitannin found in pomegranate juice with known antiproliferation and anti-angiogenesis properties. However, the antitumor effect of punicalagin on osteosarcoma requires further investigation. In the present study, the inhibitory effect of punicalagin on proliferation and invasion was evaluated in one human osteoblast cell line (hFOB1.19) and three human osteosarcoma cell lines (U2OS, MG63 and SaOS2). The cancer cell apoptosis ratio was determined using flow cytometry. NF-κB signaling in these cells was also evaluated using western blotting analysis. A subcutaneous tumor xenograft model was initiated to study the efficacy of punicalagin on osteosarcoma development and angiogenesis in vivo . Punicalagin treatment significantly decreased osteosarcoma cell proliferation and increased apoptosis. In addition, the invasion potential of these cells in a transwell assay was also dramatically suppressed in osteosarcoma cells. Punicalagin not only induced the degradation of IκBα but also the nuclear translocation of p65, suggesting the attenuation of NF-κB signaling pathway following treatment. Moreover, punicalagin markedly downregulated interleukin (IL)-6 and IL-8 levels, which was consistent with the inhibition of NF-κB signaling. An NF-κB activator could reverse these effects. Using a tumor xenograft mouse model, it was demonstrated that punicalagin exposure inhibited osteosarcoma growth and angiogenesis in vivo . These observations confirmed the suppressive effect of punicalagin against osteosarcoma malignancies. The underlying molecular mechanisms may include inhibition of the NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Punicalagin inhibited proliferation, invasion and angiogenesis of osteosarcoma through suppression of NF‑κB signaling

2020

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“…Current treatments for OS patients typically include surgery in combination with adjuvant and neo-adjuvant chemotherapeutic agents. The survival rate for metastatic OS patients is currently estimated at less than five years [ 2 ]. The existence of high levels of cellular heterogeneity, and the complexity of the molecular and genetic mechanisms associated with osteosarcomagenesis makes it extremely difficult to develop a singular therapeutic approach in the clinical setting.…”

Section: Introductionmentioning

confidence: 99%

Tumor-Associated Macrophages in Osteosarcoma: From Mechanisms to Therapy

Cersosimo

Lonardi

Bernardini

et al. 2020

IJMS

156

116

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Osteosarcomas (OSs) are bone tumors most commonly found in pediatric and adolescent patients characterized by high risk of metastatic progression and recurrence after therapy. Effective therapeutic management of this disease still remains elusive as evidenced by poor patient survival rates. To achieve a more effective therapeutic management regimen, and hence patient survival, there is a need to identify more focused targeted therapies for OSs treatment in the clinical setting. The role of the OS tumor stroma microenvironment plays a significant part in the development and dissemination of this disease. Important components, and hence potential targets for treatment, are the tumor-infiltrating macrophages that are known to orchestrate many aspects of OS stromal signaling and disease progression. In particular, increased infiltration of M2-like tumor-associated macrophages (TAMs) has been associated with OS metastasis and poor patient prognosis despite currently used aggressive therapies regimens. This review aims to provide a summary update of current macrophage-centered knowledge and to discuss the possible roles that macrophages play in the process of OS metastasis development focusing on the potential influence of stromal cross-talk signaling between TAMs, cancer-stem cells and additional OSs tumoral microenvironment factors.

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“…OS is a primary malignant bone tumor derived from mesenchymal tissue [18]. Regardless of the orthopedic surgeon, oncologist, histopathologist, radiologist, and radiotherapist are applied to therapy, the survival rate of OS remains dismal [19,20].…”

Section: Discussionmentioning

confidence: 99%

MiR-455-3p downregulation facilitates cell proliferation and invasion and predicts poor prognosis of osteosarcoma

2020

J Orthop Surg Res

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Background Osteosarcoma (OS) is one of the most primary malignant bone tumors, mainly attracting children and young adults. The microRNAs are mentioned to play vital roles in many cancers, including OS. The purpose of this study was to explore the expression and function of miR-455-3p in OS and predict the potential effects in clinical diagnosis and prognosis. Method We conducted quantitative real-time PCR to assess the expression of miR-455-3p in OS tissues and cell lines. The Cell Counting Kit-8 assay, Transwell assay, and flow cytometry were performed to assess the ability of miR-455-3p on cell proliferation, migration, invasion, and apoptosis. Kaplan–Meier curve and Cox regression analysis were used to demonstrate the survival outcome. Results This study revealed that the expression of miR-455-3p was decreased in OS tissues and cell lines. The dysregulation of miR-455-3p was in association with tumor size, distant metastasis, and clinical stage. Patients with high miR-455-3p expression had a satisfying survival rate. Multivariate Cox analysis indicated that miR-455-3p was a promising prognostic indicator. Expression of miR-455-3p could inhibit the proliferation, migration, and invasion, and facilitate apoptosis of OS cells in vitro. Conclusion These results indicated the miR-455-3p was a potential clinical therapeutic target and prognostic biomarker by suppressing the proliferation, migration, and invasion, as well as enhancing cell apoptosis.

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The efficacy and safety comparison of first-line chemotherapeutic agents (high-dose methotrexate, doxorubicin, cisplatin, and ifosfamide) for osteosarcoma: a network meta-analysis

Cited by 64 publications

References 50 publications

Punicalagin inhibited proliferation, invasion and angiogenesis of osteosarcoma through suppression of NF‑κB signaling

Punicalagin inhibited proliferation, invasion and angiogenesis of osteosarcoma through suppression of NF‑κB signaling

Tumor-Associated Macrophages in Osteosarcoma: From Mechanisms to Therapy

MiR-455-3p downregulation facilitates cell proliferation and invasion and predicts poor prognosis of osteosarcoma

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