Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species

Area of Science:

• Biochemistry
• Molecular Biology
• Cancer Research
• Pharmacology

Background:

• Reactive oxygen species (ROS) are highly reactive molecules involved in cellular signaling.
• ROS dysregulation contributes to cancer development through DNA damage or cell death induction.
• Cancer cells manipulate ROS levels to promote survival and proliferation, necessitating novel therapeutic strategies.

Purpose of the Study:

• To explore the dual role of ROS in cancer progression and regression.
• To summarize the mechanisms and achievements of shikonin-based ROS targeting in cancer therapy.
• To provide insights for future anti-tumor experimental designs and research.

Main Methods:

• Review of existing literature on ROS in cancer.
• Analysis of shikonin and its derivatives' impact on oxidative stress-related signaling pathways.
• Examination of shikonin's effects on apoptosis, necroptosis, cell cycle arrest, autophagy, and ferroptosis.

Main Results:

• Shikonin and derivatives target oxidative stress pathways to induce various forms of cancer cell death.
• These compounds can enhance chemotherapy sensitivity in drug-resistant cancer cells.
• The efficacy of ROS-targeted therapy depends on cancer type, stage, and specific ROS characteristics.

Conclusions:

• Targeting ROS, particularly with shikonin-based therapies, presents a viable strategy for cancer treatment.
• Shikonin's ability to modulate multiple cell death pathways and overcome drug resistance is significant.
• Further research is warranted to optimize shikonin-targeted ROS strategies for clinical application.