Engeletin suppresses cervical carcinogenesis in vitro and in vivo by reducing NF-κB-dependent signaling

Bai, Hongwei; Yin, Haiqin

doi:10.1016/j.bbrc.2020.03.091

Cited by 14 publications

(11 citation statements)

References 34 publications

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“…Engeletin, which is also referred to as rhamnoside of dihydrokaempferol, is a bioactive derivative of Smilax glabra rhizomilax . In prior research, engeletin has shown anti-inflammatory and antioxidant activity in vitro ( 15 ) and ability to further suppress the growth of cervical and lung cancer cells ( 16 , 17 ). Herein, we explored the protective activity of engeletin in the context of CI/R injury and assessed the underlying mechanisms whereby it regulates angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Liu

et al. 2021

Braz J Med Biol Res

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Engeletin is a natural derivative of Smilax glabra rhizomilax that exhibits anti-inflammatory activity and suppresses lipid peroxidation. In the present study, we sought to elucidate the mechanistic basis for the neuroprotective and pro-angiogenic activity of engeltin in a human umbilical vein endothelial cells (HUVECs) oxygen-glucose deprivation and reoxygenation (OGD/R) model system and a middle cerebral artery occlusion (MCAO) rat model of cerebral ischemia and reperfusion injury. These analyses revealed that engeletin (10, 20, or 40 mg/kg) was able to reduce the infarct volume, increase cerebral blood flow, improve neurological function, and bolster the expression of vascular endothelial growth factor (VEGF), vasohibin-2 (Vash-2), angiopoietin-1 (Ang-1), phosphorylated human angiopoietin receptor tyrosine kinase 2 (p-Tie2), and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) in MCAO rats. Similarly, engeletin (100, 200, or 400 nM) markedly enhanced the migration, tube formation, and VEGF expression of HUVECs in an OGD/R model system, while the VEGF receptor (R) inhibitor axitinib reversed the observed changes in HUVEC tube formation activity and Vash-2, VEGF, and CD31 expression. These data suggested that engeletin exhibited significant neuroprotective effects against cerebral ischemia and reperfusion injury in rats, and improved cerebrovascular angiogenesis by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways.

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Section: Introductionmentioning

confidence: 99%

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Liu

et al. 2021

Braz J Med Biol Res

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“…31 Thus, it is urgent to reveal reagents that can relieve the neurological injury caused by SEV. It is reported that engeletin is closely associated with various pathological processes, such as pulmonary fibrosis, 32 cervical carcinogenesis, 33 and endometritis. 34 Interestingly, Liu et al discovered that engeletin ameliorates cerebral ischemia/reperfusion injury in rats.…”

Section: Discussionmentioning

confidence: 99%

Engeletin ameliorates sevoflurane‐induced cognitive impairment by activating PPAR‐gamma in neonatal mice

Ying

Wang

2023

Neuropathology

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Sevoflurane (SEV) is a commonly used anesthetic in pediatric surgery. Recent studies reported that repeated use of SEV contributes to cognitive impairment. Engeletin has been discovered to exert anti‐inflammatory effects in various diseases. However, the detailed roles and mechanisms of engeletin in SEV‐induced cognitive dysfunction of neonatal mice remain unclear. In this study, C57BL/6 neonatal mice were randomly divided into Ctrl, SEV, SEV + Engeletin (10 mg /kg), SEV + Engeletin (20 mg/kg), and SEV + Engeletin (40 mg/kg) groups. The Morris water maze (MWM) test suggested that engeletin treatment significantly improved SEV‐induced cognitive impairment in neonatal mice. Employing ELISA and Nissl staining analysis, engeletin reduced neuroinflammation and loss of nerve cells caused by SEV, respectively. The treatment of engeletin dramatically suppressed the activation of microglia and apoptosis induced by SEV in the hippocampus of neonatal mice. Furthermore, the inhibition of PPAR‐γ obviously reversed the abovementioned effects of engeletin in the hippocampus of newborn mice. In conclusion, this study verified that engeletin notably ameliorated SEV‐induced cognitive deficiencies in neonatal mice at least partially by mediating the expression of PPAR‐γ.

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“…The results displayed that silencing hsa_circ_0000520 or CDK2 reduced weight and volume of graft tumors in nude mice. Decreased volume and weight of tumors indicate cervical cancer is ameliorated [ 24 ]. Although no circRNA-based therapeutic candidate is currently applied in the clinical setting against cervical cancer, the present experimental data highlighted the significance of hsa_circ_0000520 in cervical cancer progression as a potential biomarker of prognosis and a therapeutic target.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0000520 overexpression increases CDK2 expression via miR-1296 to facilitate cervical cancer cell proliferation

Zheng

Zhang²,

Zhang

et al. 2021

J Transl Med

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Background Circular RNA (circRNA) has been demonstrated to participate in cervical cancer development. In this study, we analyzed the role of hsa_circ_0000520 in cervical cancer. Methods Fifty-two pairs of cervical cancer and adjacent normal tissue samples were collected, and five human cervical cancer cell lines were obtained followed by the detection of hsa_circ_0000520 expression. Nuclear-cytoplasmic isolation and fluorescence in situ hybridization were performed to analyze the subcellular localization of hsa_circ_0000520 while linear RNA was digested by RNase R. Gain- or loss-of function experiments on hsa_circ_0000520 were performed, followed by detection of cell proliferation and cell cycle by EdU, Cell Counting Kit-8, colony formation assay, and flow cytometry respectively. Results Hsa_circ_0000520 and cyclin-dependent kinase 2 (CDK2) were highly expressed in cervical cancer tissues. Binding sites between microRNA-1296 (miR-1296) and hsa_circ_0000520 or CDK2 were verified. Antibody to Argonaute 2 (Ago2) could precipitate hsa_circ_0000520, indicating that hsa_circ_0000520 could competitively bind to miR-1296 via Ago2. Silencing hsa_circ_0000520 inhibited cervical cancer cell proliferation and promoted the inhibitory effects of miR-1296 on CDK2, thereby blocking cell cycle progression and promoting apoptosis. Conclusion These results support the premise that targeting hsa_circ_0000520 can be a potential approach to combat cervical cancer.

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Engeletin suppresses cervical carcinogenesis in vitro and in vivo by reducing NF-κB-dependent signaling

Cited by 14 publications

References 34 publications

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Engeletin ameliorates sevoflurane‐induced cognitive impairment by activating PPAR‐gamma in neonatal mice

Hsa_circ_0000520 overexpression increases CDK2 expression via miR-1296 to facilitate cervical cancer cell proliferation

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