Receptor Tyrosine Kinases in Osteosarcoma Treatment: Which Is the Key Target?

Tian, Zhichao; Niu, Xiaohui; Yao, Weitao

doi:10.3389/fonc.2020.01642

Cited by 61 publications

(70 citation statements)

References 156 publications

(197 reference statements)

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“…Drug resistance 7 BioMed Research International remains the obstacle to lung cancer treatment. Therapies targeting VEGFR signaling, such as Apatinib, Ramucirumab, and Axitinib, show promising effects on suppressing the proliferation and angiogenesis of gastric cancer, osteosarcoma, head and neck cancer, and NSCLC [27][28][29][30]. CED is a VEGFR tyrosine kinase inhibitor and shows anticancer potential against various types of tumours [31].…”

Section: Discussionmentioning

confidence: 99%

Cediranib Induces Apoptosis, G1 Phase Cell Cycle Arrest, and Autophagy in Non-Small-Cell Lung Cancer Cell A549 In Vitro

Guo

Liu

et al. 2021

BioMed Research International

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Lung cancer remains the leading cause of cancer death worldwide. Late diagnosis, chemoresistance, and metastasis are the main reasons for the high mortality rate of lung cancer. Therefore, the development of other treatments is urgent. Cediranib (CED), a vascular endothelial growth factor receptor (VEGFR) kinase inhibitor, shows promising antitumour activities in various cancers including lung cancer. Here, we explored the effects and the underlying molecular mechanism of CED on non-small-cell lung cancer (NSCLC) cell line A549 cells in vitro. Our results show that CED could inhibit A549 cell proliferation and cloning formation. Meanwhile, G1 phase cell cycle arrest was also found, as featured by the increased proportion of G1 phase cells as well as the reduction of G1 phase relative proteins CDK4/cyclin D1 and CDK2/cyclin E. Moreover, the ratio of LC3-II/LC3-I was elevated significantly in CED-treated groups compared with the controls. Furthermore, the expression of p-Akt, p-P38, p-Erk1/2, and p-mTOR proteins was decreased obviously in the treatment groups. These results suggest that CED could induce apoptosis and G1 phase cell cycle arrest in A549 cells. Meanwhile, CED may induce autophagy through MAPK/Erk1/2 and Akt/mTOR signal pathway in A549 cells.

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Section: Discussionmentioning

confidence: 99%

Cediranib Induces Apoptosis, G1 Phase Cell Cycle Arrest, and Autophagy in Non-Small-Cell Lung Cancer Cell A549 In Vitro

Guo

Liu

et al. 2021

BioMed Research International

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“…Therefore, one can characterize IGF-IR as one of the co-drivers of osteosarcoma progression, even though its sole inhibition is not a clinical option [231]. An alternative would be treating a subset of patients who overexpress IGF-IR with IGF-IR inhibitors as an innovative treatment approach [232].…”

Section: Data From Clinical Trials Focusing On Targeting the Igf-irmentioning

confidence: 99%

The Role of IGF/IGF-IR-Signaling and Extracellular Matrix Effectors in Bone Sarcoma Pathogenesis

Tzanakakis

Giatagana

Berdiaki

et al. 2021

Cancers

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Bone sarcomas, mesenchymal origin tumors, represent a substantial group of varying neoplasms of a distinct entity. Bone sarcoma patients show a limited response or do not respond to chemotherapy. Notably, developing efficient chemotherapy approaches, dealing with chemoresistance, and preventing metastasis pose unmet challenges in sarcoma therapy. Insulin-like growth factors 1 and 2 (IGF-1 and -2) and their respective receptors are a multifactorial system that significantly contributes to bone sarcoma pathogenesis. Whereas failures have been registered in creating novel targeted therapeutics aiming at the IGF pathway, new agent development should continue, evaluating combinatorial strategies for enhancing antitumor responses and better classifying the patients that could best benefit from these therapies. A plausible approach for developing a combinatorial strategy is to focus on the tumor microenvironment (TME) and processes executed therein. Herewith, we will discuss how the interplay between IGF-signaling and the TME constituents affects sarcomas’ basal functions and their response to therapy. This review highlights key studies focusing on IGF signaling in bone sarcomas, specifically studies underscoring novel properties that make this system an attractive therapeutic target and identifies new relationships that may be exploited. Potential direct and adjunct therapeutical implications of the extracellular matrix (ECM) effectors will also be summarized.

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“…Rather, inhibition of multiple RTKs simultaneously show a much better progress in TKI dependent osteosarcoma treatment. This is because receptor tyrosine kinases like MET, IGF-1R, AXL, PDGFRs, KIT, and FGFRs might be relevant but unimportant targets for osteosarcoma treatment [21].…”

Section: Rtk Disruption In Different Types Of Cancermentioning

confidence: 99%

Recent Advances in the Therapeutic Development of Receptor Tyrosine Kinases (RTK) against Different Types of Cancer

Patranabis¹

2021

Biochemistry

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Receptor Tyrosine Kinases (RTKs) are an important class of receptors involved in regulating different cellular functions. The usual pathway of RTK activation involves specific ligand binding, dimerization and trans-autophosphorylation. Recently, RTK has been extensively studied as they have potential applications in targeted cancer therapy. RTK-based therapeutic strategies are promising because dysfunction of RTK is connected to a variety of diseases. More specifically, RTK has been widely associated with different types of cancer and related diseases. The chapter aims to cover recent advances and challenges in RTK related research, to get an overview of the problems and possibilities associated with targeted therapy. This will help in deciphering novel therapeutic applications in the future.

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Receptor Tyrosine Kinases in Osteosarcoma Treatment: Which Is the Key Target?

Cited by 61 publications

References 156 publications

Cediranib Induces Apoptosis, G1 Phase Cell Cycle Arrest, and Autophagy in Non-Small-Cell Lung Cancer Cell A549 In Vitro

Cediranib Induces Apoptosis, G1 Phase Cell Cycle Arrest, and Autophagy in Non-Small-Cell Lung Cancer Cell A549 In Vitro

The Role of IGF/IGF-IR-Signaling and Extracellular Matrix Effectors in Bone Sarcoma Pathogenesis

Recent Advances in the Therapeutic Development of Receptor Tyrosine Kinases (RTK) against Different Types of Cancer

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