Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways

doi:10.3390/ijms23116103

Paper

Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways

Published May 29, 2022 · Hsin-Yu Ho, Ping-Ju Chen, Yi‐Ching Chuang

International Journal of Molecular Sciences

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Abstract

Nasopharyngeal carcinoma (NPC) has a higher incidence in Taiwan than worldwide. Although it is a radiosensitive malignancy, cancer recurrence is still high in the advanced stages because of its ability to induce lymph node metastasis. Picrasidine I from Picrasma quassioides has been reported as a potential drug for targeting multiple signaling pathways. The present study aimed to explore the role of picrasidine I in the apoptosis of NPC cells. Our results show that picrasidine I induced cytotoxic effects in NPC cells and caused cell cycle arrest in the sub-G1, S, and G2/M phases. Western blot analysis further demonstrated that the modulation of apoptosis through the extrinsic and intrinsic pathways was involved in picrasidine I-induced cell death. Downregulation of the ERK1/2 and Akt signaling pathways was also found in picrasidine I-induced apoptosis. Additionally, the apoptosis array showed that picrasidine I significantly increased heme oxygenase-1 (HO-1) expression, which could act as a critical molecule in picrasidine I-induced apoptosis in NPC cells. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets also revealed that the HMOX1 mRNA level (HO-1) is lower in patients with head and neck squamous carcinoma (HNSCC) and NPC than in patients without cancer. Our study indicated that picrasidine I exerts anticancer effects in NPC by modulating HO-1 via the ERK and Akt signaling pathways.

In Vitro Study

Study Snapshot

Picrasidine I induces apoptosis in nasopharyngeal carcinoma cells by modulating heme oxygenase-1 (HO-1) through the ERK and Akt signaling pathways.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways

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References

miR-140-5p Attenuates Hypoxia-Induced Breast Cancer Progression by Targeting Nrf2/HO-1 Axis in a Keap1-Independent Mechanism

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Citations

Picrasidine I Regulates Apoptosis in Melanoma Cell Lines by Activating ERK and JNK Pathways and Suppressing AKT Signaling.

Picrasidine I shows potential as a candidate for treating advanced melanoma by activating ERK and JNK pathways and suppressing AKT signaling.

Semilicoisoflavone B induces oral cancer cell apoptosis by targeting claspin and ATR‐Chk1 signaling pathways

Semilicoisoflavone B (SFB) effectively induces oral cancer cell apoptosis by targeting claspin and ATR-Chk1 signaling pathways, offering potential as a promising anticancer agent for 5FU-resistant oral cancer.

Picrasidine J, a Dimeric β-Carboline-Type Alkaloid from Picrasma quassioides, Inhibits Metastasis of Head and Neck Squamous Cell Carcinoma

Picrasidine J, a dimeric -carboline-type alkaloid from Picrasma quassioides, effectively inhibits head and neck squamous cell carcinoma (HNSCC) metastasis by inhibiting cell motility, migration, and invasion.

Hemoxygenase-1 Promotes Head and Neck Cancer Cell Viability

Hemoxygenase-1 (HO-1) promotes head and neck cancer cell viability and cell cycle progression, with its role in the disease influenced by its nuclear localization.