Apatinib Combined With Radiotherapy Enhances Antitumor Effects in an In Vivo Nasopharyngeal Carcinoma Model

Liu, Shanshan; Wu, Fei; Zhang, Yanling; Qin, Rongsheng; Zhu, Nengping; Li, Yuan; Wang, Mingting; Zeng, Qin; Xie, Danna; Li, Yinghua; Fan, Juan; Han, Yunwei

doi:10.1177/1073274820922553

Cited by 13 publications

(15 citation statements)

References 31 publications

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“…14 Currently, the main molecularly targeted therapeutic drugs with proven efficacy in the treatment of NPC are epidermal growth factor receptor (OMIM: 131550) inhibitors and vascular endothelial growth factor inhibitors. 15,16 Previous studies have demonstrated the clinical efficacy and good safety of molecular targeted therapy in NPC. However, many studies are only in the preclinical or early research stage, 17 and more phase III clinical trials are needed.…”

Section: Discussionmentioning

confidence: 99%

Expression and Biological Functions of EPC1 in Nasopharyngeal Carcinoma

et al. 2021

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Background: Comb homolog enhancer 1 (EPC1) gene is one of the important members of epigenetic inhibitor PCG family. It shows carcinogenic potential in a variety of malignant tumors, but the expression and role of EPC1 in nasopharyngeal carcinoma are unclear. The aim of this study was to explore the expression and function of enhancer of polycomb homolog 1 (EPC1) in nasopharyngeal carcinoma (NPC). Methods: The differential expression of EPC1 in the cancer tissues and cell lines of NPC was examined by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). EPC1 expression, cell proliferation, and apoptosis were detected in NPC cell lines after EPC1 silencing, and the levels of the epithelial-mesenchymal transition (EMT)-related proteins E-cadherin and vimentin were detected in NPC cells after EPC1 silencing. The study was performed at Fujian Provincial Hospital, Fujian, China, from 2018 to 2019. Results: We found that EPC1 was significantly upregulated in the cancer tissues and cell lines of NPC (P<0.001). Furthermore, knockdown of EPC1 inhibited the growth and metastasis of NPC cells. E-cadherin and vimentin were detected in NPC cells after EPC1 was knocked out. It was confirmed that inhibition of EPC1 resulted in increased E-cadherin expression (P<0.001) and decreased vimentin expression (P<0.001), suggesting that inhibition of EPC1 could inhibit the EMT in NPC cells. Conclusion: EPC1 expression was upregulated in NPC tissues and cell lines. Knockout of EPC1 effectively inhibited the growth of NPC cells, induced apoptosis, and inhibited invasion and metastasis. Inhibition of EPC1 could inhibit the EMT in NPC cells. All of the above findings support the viewpoint that EPC1 plays a pro-cancer role in NPC.

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Section: Discussionmentioning

confidence: 99%

Expression and Biological Functions of EPC1 in Nasopharyngeal Carcinoma

et al. 2021

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“…Radiotherapy combined with anti-angiogenesis therapy has been proved to be a good way to improve the anti-tumor effect in many types of cancer. Liu et al (Liu et al 2020) evaluated the therapeutic effect of radiotherapy combined with apatinib (anti-angiogenesis drug) on mouse nasopharyngeal carcinoma xenograft model, and found that the tumor inhibition effect of combined therapy was stronger than that of apatinib alone or radiotherapy alone. This is similar to the research results of Koo et al (Koo et al 2016) and Gao et al (Gao et al 2015), which all indicate the synergistic effect of anti-angiogenesis therapy on radiotherapy.…”

Section: Discussionmentioning

confidence: 99%

Role of vascular endothelial growth factor in radiotherapy resistance to esophageal squamous cell carcinoma

et al. 2022

J Cancer Res Clin Oncol

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Vascular endothelial growth factor(VEGF) is related to the radiation resistance of tumors, resulting in the failure of tumor radiotherapy. The purpose of this study was to discuss the role of VEGF in radiotherapy resistance of esophageal squamous cell carcinoma(ESCC). We used the VEGF kit by ELISA to detect the serum VEGF level of ESCC patients who only received radiotherapy. The expression of VEGF in ESCC cells after siRNA treatment was veri ed by Western blot. The sensitivity of ESCC cells to radiation after knocking down VEGF was analyzed by Clonogenic assay and Cell counting kit(CCK-8). The results showed that the level of serum VEGF in patients with ESCC before and after radiotherapy was related to the clinical response, and it was con rmed that knocking down the expression of VEGF in ESCC cells improved the sensitivity to radiation.

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“…All human experiments were approved by the Ethics Committee of the First Affiliated Hospital of Soochow University, China. On the seventh day after glioma cell inoculation, the mice that survived were intraperitoneally injected with apatinib (200 mg/kg/day) in phosphate-buffered saline (PBS) and saline solution, 4 days/week for 4 weeks [ 54 ]. The fresh drug was used for all doses for both in vitro and in vivo survival experiments.…”

Section: Methodsmentioning

confidence: 99%

Apatinib inhibits glioma cell malignancy in patient-derived orthotopic xenograft mouse model by targeting thrombospondin 1/myosin heavy chain 9 axis

et al. 2021

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We determined the antitumor mechanism of apatinib in glioma using a patient-derived orthotopic xenograft (PDOX) glioma mouse model and glioblastoma (GBM) cell lines. The PDOX mouse model was established using tumor tissues from two glioma patients via single-cell injections. Sixteen mice were successfully modeled and randomly divided into two equal groups (n = 8/group): apatinib and normal control. Survival analysis and in vivo imaging was performed to determine the effect of apatinib on glioma proliferation in vivo. Candidate genes in GBM cells that may be affected by apatinib treatment were screened using RNA-sequencing coupled with quantitative mass spectrometry, data mining of The Cancer Genome Atlas, and Chinese Glioma Genome Atlas databases, and immunohistochemistry analysis of clinical high-grade glioma pathology samples. Quantitative reverse transcription-polymerase chain reaction (qPCR), western blotting, and co-immunoprecipitation (co-IP) were performed to assess gene expression and the apatinib-mediated effect on glioma cell malignancy. Apatinib inhibited the proliferation and malignancy of glioma cells in vivo and in vitro. Thrombospondin 1 (THBS1) was identified as a potential target of apatinib that lead to inhibited glioma cell proliferation. Apatinib-mediated THBS1 downregulation in glioma cells was confirmed by qPCR and western blotting. Co-IP and mass spectrometry analysis revealed that THBS1 could interact with myosin heavy chain 9 (MYH9) in glioma cells. Simultaneous THBS1 overexpression and MYH9 knockdown suppressed glioma cell invasion and migration. These data suggest that apatinib targets THBS1 in glioma cells, potentially via MYH9, to inhibit glioma cell malignancy and may provide novel targets for glioma therapy.

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Apatinib Combined With Radiotherapy Enhances Antitumor Effects in an In Vivo Nasopharyngeal Carcinoma Model

Cited by 13 publications

References 31 publications

Expression and Biological Functions of EPC1 in Nasopharyngeal Carcinoma

Expression and Biological Functions of EPC1 in Nasopharyngeal Carcinoma

Role of vascular endothelial growth factor in radiotherapy resistance to esophageal squamous cell carcinoma

Apatinib inhibits glioma cell malignancy in patient-derived orthotopic xenograft mouse model by targeting thrombospondin 1/myosin heavy chain 9 axis

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