Anti-cancer activity of psoralidin in different malignancies
Cancer type | Model | Inhibitory concentrations | Anti-cancer activity | Mechanism of action | References |
---|---|---|---|---|---|
Prostate | PC-3, DU-145, PzHPV-7, xenograft | 45–60 µM | Induction of apoptosis↑Death receptors↓Tumor growth | ↓TNF-α mediated NF-кB signaling | [113] |
PC-3, DU-145, LNCaP, C4-2B, xenograft | 45–60 µM | ↓Cell proliferation↓Tumor growthInduction of apoptosis | ↓EGFR/MAPK signaling | [114] | |
LNCaP | 20–50 µM | Induction of apoptosis↓Cell proliferation | ↑TRAIL | [115] | |
PC-3, PzHPV-7, C4-2B | 5–20 µM | ↓Cell proliferation↓Migration, Invasion | ROS generation | [116] | |
RWPE-1, xenograft mice | 4 µM | ↓Cell proliferationInduction of apoptosisAutophagy inductionEMT Inhibition | ↓NF-кB signaling | [117] | |
Cervical | HeLa | 50 µM | Induction of apoptosisDepolarization of mitochondrial membrane potential | ↑TRAIL induced R2 death receptor | [118] |
Lung | A549 | 10–20 µM | ↓Cell proliferationAutophagy induction | ROS generation | [119] |
Breast | MCF-7, MDA-MB-231 | 10–20 µM | ↓Cell proliferationDNA damageAutophagy induction | ROS generation↑Nitrogen oxides | [120] |
Esophageal | Eca9706 | 10 µM | ↓Cell proliferationInduction of apoptosis | ↓NF-кB signaling↓PI3K/Akt signaling | [121] |
Colon | SW480 | 5–20 µM | ↓Cell proliferationInduction of apoptosis | ↓NF-кB signaling | [122] |
HT-29, HCT-116 | 0–20 µM | Induction of apoptosisdepolarization of mitochondrial membrane potential | ROS generation | [123] | |
Liver | HepG2 | 64 µM | Induction of apoptosis | ↑p53 | [124] |
HepG2, xenograft | 9 µM | ↓Cell proliferationG2/M cell cycle arrestInduction of apoptosisAutophagy induction↓Tumor growth | - | [125] | |
Osteosarcoma | 143B, MG63, orthotopic mice | 30 µM | ↓Cell proliferation↓Migration, InvasionInduction of apoptosisCell cycle arrest | ↓PI3K/Akt signaling ↓FAK | [126] |
EGFR: epidermal growth factor receptor; EMT: epithelial-mesenchymal transition; FAK: focal adhesion kinase; MAPK: mitogen-activated protein kinase; NF-кB: nuclear factor kappa B; PI3K/Akt: phosphatidylinositol 3-kinase/protein kinase B; p53: tumor protein; ROS: reactive oxygen species; TNF-α: tumor necrosis factor alpha; TRAIL: tumor necrosis factor related apoptosis inducing ligand; TRAIL-R2: TRAIL-receptor 2; -: blank cell
ACB: Conceptualization, Funding acquisition, Project administration, Resources, Supervision, Validation, Writing—review & editing. TT and ACB: Data curation, Visualization, Writing—original draft. TT, AC, DJ, UJ, NA, and CCK: Formal analysis. TT, DJ, AC, and UJ: Investigation. TT, UJ, DJ, AC, and NA: Methodology.
The authors declare that there are no conflicts of interest.
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The datasets that support the findings of this study are available from the corresponding author upon reasonable request.
This work was funded by Indian Council of Medical Research-India Cancer Research Consortium (ICMR-ICRC) [No.5/13/4/ACB/ICRC/2020/NCD-III], ICMR AdHOC [2021-10573/GENOMIC/ADHOC-BMS]; Central Council for Research in Homeopathy (CCRH) [F.No.17-30/2023-24/CCRH/Tech/Coll./DU Cervical Cancer Phase-II/498]; Institution of Eminence, University of Delhi [Ref. No./IoE/2023-24/12/FRP] to ACB is thankfully acknowledged. In addition to the above funding support, the research has received several non-funding financial support such as Senior Research Fellowship to TT [764/(CSIR-UGC NET JUNE 2019)] by University Grants Commission (UGC), and Senior Research Fellowship to DJ [09/0045/(11635)/2021-EMR-1] and AC [09/0045(12901)/2022-EMR-1] by Council of Scientific and Industrial Research (CSIR). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
© The Author(s) 2024.