Related Experiment Video
Updated: May 21, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
FAM72A Knockdown Drives Cell Mitophagy and Pyroptosis in Ovarian Cancer Via the PINK1/Parkin Pathway
Songhong Tan1, Li Wang2, Zhengmei Xu1
1Department of Gynecology, Affiliated Hengyang Hospital of Hunan Normal University & Hengyang Central Hospital, No. 31 Guanghui Road, Zhengxiang District, Hengyang City, Hunan, 421000, China.
Abstract:
This study explored the role of Family with Sequence Similarity 72 Member A (FAM72A) in regulating mitophagy and pyroptosis via the PINK1/Parkin pathway in ovarian cancer (OC). Bioinformatics analysis and clinical tissue and cell assays revealed that FAM72A was significantly overexpressed in OC. Silencing FAM72A in OC cells suppressed proliferation, invasion, and migration, while promoting apoptosis. Additionally, FAM72A knockdown increased mitochondrial ROS levels, autophagosome-mitochondria colocalization, and the LC3II/I ratio and reduced p62 expression, mitochondrial membrane potential, and ATP levels in OC cells. Downregulation of FAM72A upregulated PINK1 and Parkin expression and increased the expression of pyroptosis-related markers including NLRP3, ASC, cleaved caspase-1, IL-1β, and IL-18 in OC cells. Furthermore, the inhibitory effect of FAM72A knockdown was reversed by treating cells with mitochondrial inhibitors or by specifically knocking down PINK1. In vivo experiments confirmed that FAM72A promoted tumor growth by inhibiting the PINK1/Parkin pathway. Conclusively, FAM72A knockdown drives mitophagy and pyroptosis in OC by activating the PINK1/Parkin pathway, highlighting its potential as a therapeutic target for OC.
Insights
Family with Sequence Similarity 72 Member A (FAM72A) promotes ovarian cancer (OC) growth by inhibiting mitophagy and pyroptosis. Silencing FAM72A activates the PINK1/Parkin pathway, driving these processes and offering a potential therapeutic strategy for OC.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Ovarian cancer (OC) remains a leading cause of cancer-related deaths.
- Understanding novel molecular mechanisms regulating OC progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the role of Family with Sequence Similarity 72 Member A (FAM72A) in regulating mitophagy and pyroptosis in ovarian cancer.
- To elucidate the involvement of the PINK1/Parkin pathway in FAM72A-mediated OC progression.
Main Methods:
- Bioinformatics analysis, clinical tissue and cell assays, and in vivo experiments were employed.
- FAM72A expression and its effects on cell proliferation, invasion, migration, apoptosis, mitophagy, and pyroptosis were assessed.
- The involvement of the PINK1/Parkin pathway was investigated through gene silencing and pharmacological inhibition.
Main Results:
- FAM72A was significantly overexpressed in OC tissues and cell lines.
- FAM72A knockdown suppressed OC cell proliferation, invasion, and migration, while promoting apoptosis.
- FAM72A downregulation activated the PINK1/Parkin pathway, leading to enhanced mitophagy and pyroptosis, evidenced by increased mitochondrial ROS, autophagosome-mitochondria colocalization, LC3II/I ratio, and pyroptosis markers (NLRP3, ASC, cleaved caspase-1, IL-1β, IL-18), and decreased p62, mitochondrial membrane potential, and ATP levels.
- Inhibition of the PINK1/Parkin pathway reversed the anti-tumor effects of FAM72A knockdown.
Conclusions:
- FAM72A promotes ovarian cancer progression by suppressing mitophagy and pyroptosis through the inhibition of the PINK1/Parkin pathway.
- FAM72A knockdown induces mitophagy and pyroptosis by activating the PINK1/Parkin pathway, suggesting FAM72A as a potential therapeutic target for ovarian cancer.
Related Concept Videos
The Intrinsic Apoptotic Pathway
Abnormal Proliferation
PI3K/mTOR/AKT Signaling Pathway
The Extrinsic Apoptotic Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Overview of Cell Death
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...

