Cell Proliferation and Apoptosis-Related Genes Affect the Development of Human Nasopharyngeal Carcinoma Through PI3K/AKT Signaling Pathway

Li, Wei; Ma, Hui‐Ping; Liu, Minglei

doi:10.1007/s12033-021-00357-0

Cited by 3 publications

(2 citation statements)

References 54 publications

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“…Therefore, we focused on the PI3K-AKT signaling pathway to explore the mechanism underlying the effects of compound 6e on KB cells. PI3K/AKT pathway plays an important role in a variety of biological processes, such as cell growth, proliferation, differentiation and apoptosis ( Noorolyai et al, 2019 ; Xie et al, 2019 ; Dong et al, 2020 ; Li et al, 2021 ). Western blotting demonstrated that compound 6e significantly reduced the pAKT/AKT ratio ( Figure 9A ), down-regulating the level of AKT phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

Design, synthesis and anticancer activity studies of 3-(coumarin-3-yl)-acrolein derivatives: Evidenced by integrating network pharmacology and vitro assay

Chen

Cai

et al. 2023

Front. Pharmacol.

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Coumarin derivatives have diverse structures and show various significant biological activities. Aiming to develop more potent coumarin derivatives for cancer treatment, a series of coumarin acrolein hybrids were designed and synthesized by using molecular hybridization approach, and investigated for their antiproliferative activity against A549, KB, Hela and MCF-7 cancer cells as well as HUVEC and LO2 human normal cells. The results indicated that most of the synthesized compounds displayed remarkable inhibitory activity towards cancer cells but low cytotoxicity on normal cells. Among all the compounds, 5d and 6e were the most promising compounds against different cancer cell lines, especially for A549 and KB cells. The preliminary action mechanism studies suggested that compound 6e, the representative compound, was capable of dose-dependently suppressing migration, invasion and inducing significant apoptosis. Furthermore, the combined results of network pharmacology and validation experiments revealed that compound 6e induced mitochondria dependent apoptosis via the PI3K/AKT-mediated Bcl-2 signaling pathway. In summary, our study indicated compound 6e could inhibit cell proliferation, migration, invasion and promote cell apoptosis through inhibition of PI3K/AKT signaling pathway in human oral epidermoid carcinoma cells. These findings demonstrated the potential of 3-(coumarin-3-yl)-acrolein derivatives as novel anticancer chemotherapeutic candidates, providing ideas for further development of drugs for clinical use.

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Section: Discussionmentioning

confidence: 99%

Design, synthesis and anticancer activity studies of 3-(coumarin-3-yl)-acrolein derivatives: Evidenced by integrating network pharmacology and vitro assay

Chen

Cai

et al. 2023

Front. Pharmacol.

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“…Analysis of the network's topological variables revealed that STAT3, JUN, and AKT1 genes were highly ranked throughout the network. STAT3 is a key signaling protein that a multitude of growth factors and cytokines use to elicit diverse biological outcomes, including cellular growth, differentiation, and survival 13 . JUN acts on the AP-1 (c-JUN) signaling pathway and plays an important role in in ammatory cell proliferation and differentiation, and its expression is associated with the secretion of cytokines and in ammatory mediators [14][15] .…”

Section: Discussionmentioning

confidence: 99%

Jianpi Qinghua Sanyu Decoction attenuates insulin-like growth factor 1-induced GES-1 cell proliferation by suppressing the AKT pathway based on network pharmacology analysis

Liu

Zhao

Lin

et al. 2023

Preprint

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Raised erosive gastritis (REG) is a gastric mucosal lesion with characteristic radiological and endoscopic features. Jianpi Qinghua Sanyu Decoction (JPQHSYD) may be effective against REG, but its therapeutic effects and underlying molecular mechanisms have yet to be investigated. A network pharmacology analysis was performed to identify itsJPQHSYD active ingredients, potential targets, and pathways in REG treatment. Following database mining, our current study identified 245 compounds and 320 potential targets, as well as 94 common targets with REG. The construction of a traditional Chinese medicine (TCM) comprehensive network (Drug-Ingredients-Gene symbols-Disease network) identified ten potentially active compounds (including Quercetin) and 35 potential targets (including AKT1), as well as enriched signaling pathways (including cell proliferation and phosphatidylinositol 3-kinase and protein kinase B (PI3K/Akt)). In vitro studies revealed that JPQHSYD significantly inhibits cell growth and viability while also down-regulating p-AKT, Bcl-2, CDK4, and CyclinD1 expression and up-regulating Bax protein levels in insulin-like growth factor 1 (IGF-1)-stimulated GES-1 cells. This study provides novel insights into the mechanism of action of JPQHSYD in REG treatment, implying that suppressing the AKT pathway may be one of the essential underlying anti-REG mechanisms of JPQHSYD.

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Exploring the pharmacological mechanisms of Biyan Qingdu Granula in the treatment after nasopharyngeal carcinoma radiotherapy based on UPLC/Q-TOF MS, network pharmacology and molecular docking

Yi,

Lv,

Zhang

et al. 2024

Journal of Pharmaceutical and Biomedical Analysis

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Cell Proliferation and Apoptosis-Related Genes Affect the Development of Human Nasopharyngeal Carcinoma Through PI3K/AKT Signaling Pathway

Cited by 3 publications

References 54 publications

Design, synthesis and anticancer activity studies of 3-(coumarin-3-yl)-acrolein derivatives: Evidenced by integrating network pharmacology and vitro assay

Design, synthesis and anticancer activity studies of 3-(coumarin-3-yl)-acrolein derivatives: Evidenced by integrating network pharmacology and vitro assay

Jianpi Qinghua Sanyu Decoction attenuates insulin-like growth factor 1-induced GES-1 cell proliferation by suppressing the AKT pathway based on network pharmacology analysis

Exploring the pharmacological mechanisms of Biyan Qingdu Granula in the treatment after nasopharyngeal carcinoma radiotherapy based on UPLC/Q-TOF MS, network pharmacology and molecular docking

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