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Updated: Jul 15, 2026

Flow Cytometric Analysis of Apoptotic Biomarkers in Actinomycin D-Treated SiHa Cervical Cancer Cells
Published on: August 26, 2021
AKAP12 induces apoptotic cell death in human fibrosarcoma cells by regulating CDKI-cyclin D1 and caspase-3 activity
Dae-Kwan Yoon1, Chul-Ho Jeong, Hyoung Oh Jun
1NeuroVascular Coordination Research Center, Division of Pharmaceutical Biosciences, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Abstract:
AKAP12 (A-Kinase anchoring protein 12) is a protein kinase C substrate and a potential tumor suppressor. AKAP12 is down-regulated by several oncogenes and strongly suppressed in various cancers including prostate, ovarian and breast cancers. AKAP12 acts as a regulator of mitogenesis by anchoring key signal proteins such as PKA, PKC, and cyclins. In this study, AKAP12 was found to suppress tumor cell viability by inducing apoptosis via caspase-3 in HT1080 cells. This AKAP12-induced apoptosis was associated with a decreased expression of Bcl-2 and increased expression of Bax. Moreover, AKAP12-transfectant strongly induced the expression of Cip1/p21 and Kip1/p27, but resulted in a decrease in cyclin D1 involved in G(1) progression. Accordingly, these results suggest that AKAP12 may play an important role in tumor growth suppression by inducing apoptosis with the regulation of multiple molecules in the cell cycle progression.
Insights
A-Kinase anchoring protein 12 (AKAP12) suppresses tumor cell viability by inducing apoptosis and regulating cell cycle progression. This protein kinase C substrate is down-regulated in various cancers, suggesting its role as a tumor suppressor.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- A-Kinase anchoring protein 12 (AKAP12) functions as a protein kinase C substrate and a potential tumor suppressor.
- AKAP12 is frequently downregulated by oncogenes and suppressed in prostate, ovarian, and breast cancers.
- AKAP12 regulates mitogenesis by anchoring key signaling proteins like PKA, PKC, and cyclins.
Purpose of the Study:
- To investigate the role of AKAP12 in suppressing tumor cell viability.
- To elucidate the molecular mechanisms underlying AKAP12-mediated tumor suppression, focusing on apoptosis and cell cycle regulation.
Main Methods:
- Transfection of HT1080 cells with AKAP12.
- Analysis of apoptosis markers, including caspase-3, Bcl-2, and Bax expression.
- Assessment of cell cycle regulatory proteins, such as Cip1/p21, Kip1/p27, and cyclin D1.
Main Results:
- AKAP12 transfection suppressed tumor cell viability in HT1080 cells by inducing apoptosis via caspase-3.
- AKAP12-induced apoptosis correlated with decreased Bcl-2 and increased Bax expression.
- AKAP12 significantly upregulated Cip1/p21 and Kip1/p27 while decreasing cyclin D1, inhibiting G1 cell cycle progression.
Conclusions:
- AKAP12 plays a critical role in tumor growth suppression.
- AKAP12 induces apoptosis and regulates cell cycle progression through modulation of key molecular targets.
- AKAP12 represents a potential therapeutic target for cancer treatment.
Related Concept Videos
The Intrinsic Apoptotic Pathway
The Extrinsic Apoptotic Pathway
Caspases
Inhibition of Cdk Activity
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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...
