Leptin and apoptosis inhibitor soluble fas antigen in the serum of patients with osteosarcoma and neuroectodermal bone tumors

Kushlinskii, N. E.; Solov’ev, Yu. N.; Бабкина, И. В.; Abbasova, S. G.; Коstanyan, I. A.; Липкин, В. М.; Trapeznikov, N. N.

doi:10.1007/bf02439813

Cited by 9 publications

(4 citation statements)

References 11 publications

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“…Acquired resistance protects osteosarcoma tumor cells against apoptosis induced by radiotherapy, chemotherapy and combined therapy in the treatment of tumors (36,37). Reducing the apoptotic resistance of cancer cells and tumors tissues will contribute to the clinical treatment for of with osteosarcoma who have undergone oncotherapy and other comprehensive treatments (38,39). In this study, the data indicated that miR-124 transfection promoted apoptosis of osteosarcoma cells, potentially via regulation of P53, Bcl-2, Apaf-1 and Bad expression.…”

Section: Discussionmentioning

confidence: 69%

MicroRNA-124 suppresses growth and aggressiveness of osteosarcoma and inhibits TGF-β-mediated AKT/GSK-3β/SNAIL-1 signaling

Jiang

Zhang

2018

Mol Med Report

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Osteosarcoma is one of the most common malignant tumors in adolescent populations and the prognosis remains incompletely understand. Previous reports have demonstrated that microRNA‑124 (miR‑124) has inhibitory effects on various human malignancies and is associated with tumor progression. However, the clinical significance and potential mechanisms of miR‑124 in the progression of osteosarcoma is not clearly understood. In this study, the potential molecular mechanism of miR‑124 in osteosarcoma tumorigenesis, growth and aggressiveness was investigated. The growth, proliferation, apoptosis, migration and invasion of osteosarcoma cells were investigated following miR‑124 transfection were determined by colony formation assay, western blotting, immunofluorescence, migration/invasion assays and reverse transcription‑quantitative polymerase chain reaction. In vivo anti‑cancer effects of miR‑124 were analyzed by a tumor growth assay, immunohistochemistry and survival rate observations. The results demonstrated that miR‑124 transfection significantly decreased integrin expression in osteosarcoma cells, and further inhibited growth, proliferation, migration and invasion of osteosarcoma cells. Flow cytometry assays indicated that miR‑124 transfection attenuated apoptosis resistance of osteosarcoma to tunicamycin, potentially via the downregulation of P53 and Bcl‑2 apoptosis regulator expression. Mechanistic assays demonstrated that miR‑124 transfection suppressed TGF‑β expression in osteosarcoma. An animal study revealed that tumor growth was reduced in tumor cells transfected with miR‑124 compared with control cells, and the survival rate was prolonged in mice with miR‑124 transfected xenografts compared with control tumors. In conclusion, these results indicate that miR‑124 transection inhibits the growth and aggressive of osteosarcoma, potentially via suppression of TGF‑β‑mediated AKT/GSK‑3β/snail family transcriptional repressor 1 (SNAIL‑1) signaling, suggesting miR‑124 may be a potential anti‑cancer agent/target for osteosarcoma therapy.

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Section: Discussionmentioning

confidence: 69%

MicroRNA-124 suppresses growth and aggressiveness of osteosarcoma and inhibits TGF-β-mediated AKT/GSK-3β/SNAIL-1 signaling

Jiang

Zhang

2018

Mol Med Report

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“…Resistance to apoptosis is the greatest obstacle to the treatment of human cancer ( 32 , 33 ). Decreasing the apoptosis-resistance of cancer cells and tumors tissues may improve the clinical treatment outcomes of patients with osteosarcoma who have undergone oncotherapy and other comprehensive treatments ( 34 , 35 ). In recent years, TRIM-14 was identified as an oncogene that promotes tumor growth, aggressiveness and tumor angiogenesis; however, knockdown of TRIM-14 expression can significantly inhibit tumor growth, migration, invasion and tumor angiogenesis in human colorectal cancer cells ( 36 ).…”

Section: Discussionmentioning

confidence: 99%

Target therapy of TRIM-14 inhibits osteosarcoma aggressiveness through the nuclear factor-κB signaling pathway

Zhang

Zhao

et al. 2017

Exp Ther Med

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Osteosarcoma is the most common cause of cancer-associated mortality and the prognosis is yet to be fully elucidated due to the paucity of effective therapeutic targets that significantly influence the quality of life and mean survival rates of patients with osteosarcoma. Studies have showed that tripartite motif-containing (TRIM)-14 is a member of the TRIM protein family that has a vital role in tumor progression and metastasis and promotes angiogenesis, invasion and apoptotic resistance of bone cancer. In this study, a chimeric antibody targeting TRIM-14 (Chanti-TRIM) was constructed and the molecular mechanism of target therapy for TRIM-14 was investigated in osteosarcoma cells and xenograft mice. The growth, migration and invasion properties of U-2OS cells were analyzed following incubation with 10–160 mg/ml Chanti-TRIM. Apoptosis of U-2OS cells was detected after Chanti-TRIM treatment. Matrix metalloproteinase (MMP)-9-mediated nuclear factor-κB (NF-κB) signal pathway was analyzed in U-2OS cells treated with Chanti-TRIM. The inhibitory efficacy of Chanti-TRIM was studied in U-2OS-bearing xenograft mice. Our results demonstrated that neutralizing TRIM-14 expression markedly inhibited the growth, migration and invasion of osteosarcoma cells, in vitro and in vivo. We found that TRIM-14 depletion decreased cell viability and induced cells apoptosis in vitro. In addition, we identified Chanti-TRIM inhibited growth and promoted apoptosis induced by cisplatin through MMP-9-mediated NF-κB signal pathway. Furthermore, we observed that Chanti-TRIM treatment inhibited osteosarcoma growth in vivo. Histological analysis indicated that apoptotic bodies were increased and NF-κB nuclear translocation factors, including Ikkβ, p65 and IkBα, were decreased in tumors treated by Chanti-TRIM. In conclusion, these results showed that Chanti-TRIM markedly inhibited the progression of osteosarcoma, suggesting Chanti-TRIM may be a potential anti-cancer agent that functions via the activation of the NF-κB pathway for osteosarcoma.

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“…Immune surveillance of OS may be modulated in situ by the neural and the endocrine systems. Indeed, leptin, which is elevated in subjects with OS (Kushlinskii et al, 2000), plays a significant role in regulating circadian neuroendocrine (e.g., cortisol) and cytokine (e.g., IL-6, IFN) production (Prolo et al, 1998). Taken together, these avenues of basic research suggest novel interventions for patients with mandibular and maxillary OS, or with OS outside of the confines of the head and neck region.…”

Section: Discussionmentioning

confidence: 99%

Neuroendocrine-Immune Surveillance of Osteosarcoma: Emerging Hypothesis

et al. 2003

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Osteosarcoma is a bone-forming cancer predominantly found in children and adolescents more often than in adults. Osteosarcoma of the gnathic apparatus is relatively rare in the young population, and this condition becomes a concern of clinical dentists for predominantly the middle-aged and aging patient groups. Osteosarcomas are invaded by lymphocytes, which exhibit signs of activation. The immune processes that are engaged within the malignant bone matrix involve the production of cytokines, which regulate the process of apoptotic programmed cell death. This paper discusses the mechanisms by which apoptosis of osteosarcoma cells is modulated by the neuroendocrine-immune system, and potential physiological implications.

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Leptin and apoptosis inhibitor soluble fas antigen in the serum of patients with osteosarcoma and neuroectodermal bone tumors

Cited by 9 publications

References 11 publications

MicroRNA-124 suppresses growth and aggressiveness of osteosarcoma and inhibits TGF-β-mediated AKT/GSK-3β/SNAIL-1 signaling

MicroRNA-124 suppresses growth and aggressiveness of osteosarcoma and inhibits TGF-β-mediated AKT/GSK-3β/SNAIL-1 signaling

Target therapy of TRIM-14 inhibits osteosarcoma aggressiveness through the nuclear factor-κB signaling pathway

Neuroendocrine-Immune Surveillance of Osteosarcoma: Emerging Hypothesis

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