Paiteling induces apoptosis of cervical cancer cells by down-regulation of the E6/E7-Pi3k/Akt pathway: A network pharmacology

Liu, Yunhua; Zheng, Pengfei; Jiao, Tingting; Zhang, Mengmeng; Wu, Yingjie; Zhang, Xinjiang; Wang, Shuyue; Zhao, Zongjiang

doi:10.1016/j.jep.2022.116062

Cited by 7 publications

(1 citation statement)

References 49 publications

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“…IGF-1 promotes cancer development mainly via the PI3K/AKT (24,25) and Ras/MAPK pathways (26). Disorders related to the PI3K/AKT signaling pathway occur in various human diseases, including cancer (27,28), diabetes (29), cardiovascular (30) and neurological disease (31). In cancer, activated AKT regulates different cellular biological functions in the following ways: i) regulation of cell growth by activating mTOR and downstream molecules (25); ii) regulation of cell proliferation by phosphorylating p27 (32) iii) direct inhibition of cell apoptosis by inhibiting apoptotic proteins (such as BAX) (33) or transcription factors (such as FOXO) (34) iv) participation in cell migration and invasion by regulating E-cadherin and vimentin (35) and v) regulation of NF-κB signaling pathway via phosphorylation of IKK (36).…”

Section: Discussionmentioning

confidence: 99%

Analysis of the expression and mechanism of follistatin‑like protein 1 in cervical cancer

Liu,

Zhang,

2023

Oncol Rep

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The abnormal expression of follistatin-like protein 1 (FSTL1) in various tumors is a crucial regulator of the biological process of tumorigenesis. Nonetheless, the regulatory role of FSTL1 in cervical cancer is yet to be elucidated. Hence, the present study aimed to explore the expression, function, and molecular mechanism of FSTL1 in cervical cancer. The expression of FSTL1 in normal and cervical cancer tissues was examined using quantitative reverse transcription-polymerase chain reaction and immunohistochemistry assays. The effects of abnormal expression of FSTL1 on cervical cancer cells were assessed using colony formation, MTT, wound-healing, Transwell, apoptosis, and nude mouse tumorigenicity assays. FSTL1-related molecular mechanisms were screened using gene chip analysis. Western blotting analysis was used to verify the regulatory mechanisms of FSTL1 in cervical cancer. The results indicated that the expression of FSTL1 was downregulated in cervical cancer tissues and that its downregulation was associated with tumor differentiation, pathologic type, and infiltration depth. Moreover, FSTL1 inhibited the proliferation, migration, and invasion of cervical cancer cells as well as xenograft tumor growth and promoted cell apoptosis. In addition, the findings of gene chip analysis suggested that the differentially expressed genes of FSTL1 were predominantly enriched in multiple signaling pathways, of which the insulin-like growth factor (IGF)-1 signaling pathway was significantly activated. Western blotting suggested the involvement of FSTL1 in the regulation of the IGF-1R/PI3K/AKT/BCL-2 signaling pathway. These data establish the downregulation of FSTL1 in cervical cancer tissues. FSTL1 inhibited the proliferation, migration, and invasion of cervical cancer cells and promoted their apoptosis. Furthermore, xenograft tumor growth in nude mice was inhibited. FSTL1 may be involved in the regulation of the IGF-1R/PI3K/AKT/BCL-2 signaling pathway in cervical cancer. Therefore, FSTL1 may be employed as a novel biomarker to determine the extent of disease progression in patients with cervical cancer.

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Section: Discussionmentioning

confidence: 99%

Analysis of the expression and mechanism of follistatin‑like protein 1 in cervical cancer

Liu,

Zhang,

2023

Oncol Rep

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Synergistic cytotoxicity and in vitro antioxidant activity of hederagenin and its glycoside from quinoa

Zhang,

Zhao,

et al. 2024

Biotech and App Biochem

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Although a series of studies confirm the bioactivities of hederagenin and its glycosides, their synergistic effects and potential mechanisms are still worthy of further exploration. This work investigated the synergistic cytotoxicity and in vitro antioxidant activity of hederagenin and hederagenin 28‐O‐β‐d‐glucopyranoside (28‐Glc‐hederagenin). Hederagenin and 28‐Glc‐hederagenin inhibited HeLa cell growth and their combination further strengthened this effect. The combination of hederagenin and 28‐Glc‐hederagenin significantly increased the rate of apoptotic cells, suggesting the presence of a synergistic effect between the two substances. This combination also enhanced in vitro antioxidant activity compared with individual treatments. A network pharmacology and molecular docking‐based approach was performed to explore the underlying mechanisms of hederagenin and 28‐Glc‐hederagenin against cervical cancer and oxidant damage. This work identified 18 related Kyoto Encyclopedia of Genes and Genome pathways, 202 related biological process terms, 17 related CC terms, and 35 related molecular function terms and then revealed 30 nodes and 196 edges. Subsequently, two highly connected clusters and the top four targets were identified. Molecular docking showed potent binding affinity of hederagenin and 28‐Glc‐hederagenin toward core targets associated with both cervical cancer and oxidant damage. This work may provide scientific basis for the combined use of hederagenin and its glycosides as dietary supplements.

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Comparative analysis of Paiteling a traditional Chinese medicine (TCM) and CO2 laser therapy for high-risk HPV-associated with LSIL (CIN1) lesions

Cobbinah,

Zheng Zheng,

Oklah

et al. 2024

European Journal of Obstetrics & Gynecology and Reproductiv

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Paiteling induces apoptosis of cervical cancer cells by down-regulation of the E6/E7-Pi3k/Akt pathway: A network pharmacology

Cited by 7 publications

References 49 publications

Analysis of the expression and mechanism of follistatin‑like protein 1 in cervical cancer

Analysis of the expression and mechanism of follistatin‑like protein 1 in cervical cancer

Synergistic cytotoxicity and in vitro antioxidant activity of hederagenin and its glycoside from quinoa

Comparative analysis of Paiteling a traditional Chinese medicine (TCM) and CO2 laser therapy for high-risk HPV-associated with LSIL (CIN1) lesions

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