Molecular and metabolic mechanisms of bufalin against lung adenocarcinoma: New and comprehensive evidences from network pharmacology, metabolomics and molecular biology experiment

Shi, Shulong; Zhao, Sihao; Tian, Xinchen; Liu, Fen; Lü, Xin; Zang, Hengchang; Li, Feng; Xiang, Lei; Li, Luning; Jiang, Shulong

doi:10.1016/j.compbiomed.2023.106777

Computers in Biology and Medicine

2023

DOI: 10.1016/j.compbiomed.2023.106777

|View full text |Cite

Molecular and metabolic mechanisms of bufalin against lung adenocarcinoma: New and comprehensive evidences from network pharmacology, metabolomics and molecular biology experiment

Shulong Shi

Sihao Zhao

Xinchen Tian

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

2025

Publication Types

Select...

Article5

Relationship

Self Cite0

Independent5

Authors

Journals

Cited by 19 publications

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

PLEK2 activates the PI3K/AKT signaling pathway to drive lung adenocarcinoma progression by upregulating SPC25

Zhang,

Yu,

et al. 2024

Cell Biology International

View full text Add to dashboard Cite

Lung adenocarcinoma (LUAD) is the most common subtype of NSCLC, characterized by poor prognosis and frequently diagnosed at advanced. While previous studies have demonstrated pleckstrin‐2 (PLEK2) as aberrantly expressed and implicated in tumorigenesis across various tumor types, including LUAD, the molecular mechanisms underlying PLEK2‐mediated LUAD progression remain incompletely understood. In this study, we obtained data from The Cancer Genome Atlas (TCGA) database to assess PLEK2 expression in LUAD, a finding further confirmed through analysis of human tissue specimens. PLEK2‐silenced LUAD cellular models were subsequently constructed to examine the functional role of PLEK2 both in vitro and in vivo. Our results showed elevated PLEK2 expression in LUAD, correlating with poor patients' prognosis. PLEK2 knockdown led to a significant suppression of LUAD cell proliferation and migration, accompanied by enhanced apoptosis. Moreover, tumor growth in mice injected with PLEK2‐silencing LUAD cells was impaired. Gene expression profiling and Co‐IP assays suggested direct interaction between PLEK2 and SPC25, with downregulation of SPC25 similarly impairing cell proliferation and migration. Additionally, we revealed phosphoinositide 3‐kinase (PI3K)/AKT signaling activation as requisite for PLEK2‐induced malignant phenotypes in LUAD. Collectively, our findings underscore PLEK2's oncogenic potential in LUAD, suggesting its utility as a prognostic indicator and therapeutic target for LUAD management.

show abstract

PLEK2 activates the PI3K/AKT signaling pathway to drive lung adenocarcinoma progression by upregulating SPC25

Zhang,

Yu,

et al. 2024

Cell Biology International

View full text Add to dashboard Cite

show abstract

Pharmacological insights and role of bufalin (bufadienolides) in inflammation modulation: a narrative review

Kaur,

Devi,

Sharma

et al. 2024

Inflammopharmacol

View full text Add to dashboard Cite

ACE inhibitors from Suaeda salsa: 3D-QSAR modeling, metabolomics, molecular docking and molecular dynamics simulations

Yue,

Gu,

Zhang

et al. 2024

In Silico Pharmacol.

View full text Add to dashboard Cite

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Molecular and metabolic mechanisms of bufalin against lung adenocarcinoma: New and comprehensive evidences from network pharmacology, metabolomics and molecular biology experiment

Cited by 19 publications

References 39 publications

PLEK2 activates the PI3K/AKT signaling pathway to drive lung adenocarcinoma progression by upregulating SPC25

PLEK2 activates the PI3K/AKT signaling pathway to drive lung adenocarcinoma progression by upregulating SPC25

Pharmacological insights and role of bufalin (bufadienolides) in inflammation modulation: a narrative review

ACE inhibitors from Suaeda salsa: 3D-QSAR modeling, metabolomics, molecular docking and molecular dynamics simulations

Contact Info

Product

Resources

About