Endostar Synergizes with Radiotherapy to Inhibit Angiogenesis of Cervical Cancer in a Subcutaneous Xenograft Mouse Model

Xu, Z.; Zhao, Xin; Hu, Shu; Luo, Wei; Dong, Yaqing; Xu, Lei; Zhu, Haoxiang; Zhao, Qian; Yin, Li

doi:10.31083/j.fbl2708238

Cited by 5 publications

(2 citation statements)

References 34 publications

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“…Previous studies have shown that endostar blocked pathological angiogenesis to inhibit tumor formation and metastasis by binding with multiple targets [42]. It was found that endostar combined with radiotherapy or chemotherapy had excellent application prospects [22,43]. In this study, we evaluated the therapeutic effect of endostar in combination with cisplatin in NSCLC mice.…”

Section: Discussionmentioning

confidence: 99%

Multi-omics sequencing revealed endostar combined with cisplatin treated non small cell lung cancer via anti-angiogenesis

Wang,

Ren

2024

BMC Cancer

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Background Endostar, an anti-angiogenic drug, has been approved for treating non-small cell lung cancer (NSCLC). At present, endostar combined with radiotherapy or chemotherapy has achieved ideal results in the treatment of some tumors, but there is a lack of application and study in NSCLC. This study investigated the therapeutic effect and potential mechanism of endostar combined with cisplatin (EC) in NSCLC. Methods HE staining, TUNEL staining, immunofluorescence, colony formation ability, and cell migration ability were used to evaluate the anti-tumor activity of EC. The expressions of FMOD, VEGF, FGF-2, and PDGF-B were detected by western blotting and qPCR. The target of combination therapy was analyzed by m6A sequencing and RNA sequencing. METTL3 knockdown and overexpressed A549 cells were constructed and co-cultured with HUVECs to further evaluate the effect of METLL3 on combination therapy. Results Combination therapy significantly reduced the colony formation and migration ability of NSCLC cells, induced cell apoptosis, and inhibited the tube formation ability of HUVECs. The results of m6A sequencing and RNA sequencing showed that the EC could down-regulate the expression level of FMOD in tumor tissues, which might be related to the reduction of its m6A methylation modification regulatory enzyme METTL3. Restricting FMOD expression could reduce the expression of FGF2, TGF-β1, VEGF and PDGF-B. Moreover, overexpression of METTLE almost abolished the anti-tumor effect of EC and promoted angiogenesis. Conclusions Endostar combined with cisplatin might exert anti-tumor effects by down-regulating the expression of METTL3 and FMOD.

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Section: Discussionmentioning

confidence: 99%

Multi-omics sequencing revealed endostar combined with cisplatin treated non small cell lung cancer via anti-angiogenesis

Wang,

Ren

2024

BMC Cancer

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“…(23) VEGF assumes a significant part in cancer angiogenesis, and lymphangiogenesis and animates the development of veins in growth tissue, expanding the conveyance of oxygen and supplements to the cancer and in this way advancing its multiplication and metastasis. (24,25)…”

Section: Serum Vegf-a Levels Before Therapy With Chemotherapy Responsementioning

confidence: 99%

Relationship between Serum Vascular Endothelial Growth Factor-A Levels and Response to Chemotherapy in Cervical Cancer

Milha Nidiya Marni,

Mulawardhana,

Wardhani

2024

Salud, Ciencia y Tecnología

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Introduction: Cervical cancer ranks second in gynecological cancer worldwide. 62-82% of cervical cancer patients present at an advanced stage and respond poorly to treatment. Assessment of chemotherapy response requires examination of the biomarker Vascular endothelial growth factor-A (VEGF-A), which is the main regulator of the abnormal angiogenesis process. Objectives: This study aims to analyze the relationship between serum VEGF-A levels and the response to neoadjuvant chemotherapy in cervical cancer patients. Methods: This research is Quasi-Experimental, pretest and posttest without control. Total sample: 30 stages IIIB cervical cancer patients underwent a pretest before cisplatin chemotherapy by measuring cervical lesions using ultrasound and serum VEGF-A levels using ELISA. 3 weeks after the third cycle of chemotherapy, a posttest examination is carried out like the pretest examination. Results: The results showed a significant reduction in serum VEGF-A levels and cervical lesion diameter after chemotherapy (p=0.032), (p=0.000). In response to neoadjuvant chemotherapy, 21 patients responded negatively, and 9 responded positively. High levels of VEGF-A before chemotherapy gave a negative response (p=0.042) and low levels of VEGF-A after chemotherapy gave a positive response (p=0.049). Conclusions: This study concludes that there is a relationship between high serum VEGF-A levels before chemotherapy with a negative response and low serum VEGF-A levels after chemotherapy with a positive response in cervical cancer patients.

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Proteoglycans of basement membranes: Crucial controllers of angiogenesis, neurogenesis, and autophagy

Mongiat,

Pascal,

Poletto

et al. 2024

Proteoglycan Research

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Antiangiogenic therapy is an established method for the treatment of several cancers and vascular‐related diseases. Most of the agents employed target the vascular endothelial growth factor A, the major cytokine stimulating angiogenesis. However, the efficacy of these treatments is limited by the onset of drug resistance. Therefore, it is of fundamental importance to better understand the mechanisms that regulate angiogenesis and the microenvironmental cues that play significant role and influence patient treatment and outcome. In this context, here we review the importance of the three basement membrane (BM) heparan sulfate proteoglycans (HSPGs), namely perlecan, agrin, and collagen XVIII. These HSPGs are abundantly expressed in the vasculature and, due to their complex molecular architecture, they interact with multiple endothelial cell receptors, deeply affecting their function. Under normal conditions, these proteoglycans exert proangiogenic functions. However, in pathological conditions such as cancer and inflammation, extracellular matrix remodeling leads to the degradation of these large precursor molecules and the liberation of bioactive processed fragments displaying potent angiostatic activity. These unexpected functions have been demonstrated for the C‐terminal fragments of perlecan and collagen XVIII, endorepellin, and endostatin. These bioactive fragments can also induce autophagy in vascular endothelial cells which contributes to angiostasis. Overall, BM proteoglycans deeply affect angiogenesis counterbalancing proangiogenic signals during tumor progression and represent possible means to develop new prognostic biomarkers and novel therapeutic approaches for the treatment of solid tumors.

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Endostar Synergizes with Radiotherapy to Inhibit Angiogenesis of Cervical Cancer in a Subcutaneous Xenograft Mouse Model

Cited by 5 publications

References 34 publications

Multi-omics sequencing revealed endostar combined with cisplatin treated non small cell lung cancer via anti-angiogenesis

Multi-omics sequencing revealed endostar combined with cisplatin treated non small cell lung cancer via anti-angiogenesis

Relationship between Serum Vascular Endothelial Growth Factor-A Levels and Response to Chemotherapy in Cervical Cancer

Proteoglycans of basement membranes: Crucial controllers of angiogenesis, neurogenesis, and autophagy

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