PDCD4 Knockdown Induces Senescence in Hepatoma Cells by Up-Regulating the p21 Expression
Open accessAbstract
While the over-expression of tumor suppressor programmed cell death 4 (PDCD4) induces apoptosis, it was recently shown that PDCD4 knockdown also induced apoptosis. In this study, we examined the cell cycle regulators whose activation is affected by PDCD4 knockdown to investigate the contribution of PDCD4 to cell cycle regulation in three types of hepatoma cells: HepG2, Huh7 (mutant p53 and p16-deficient), and Hep3B (p53- and Rb-deficient). PDCD4 knockdown suppressed cell growth in all three cell lines by inhibiting Rb phosphorylation via down-regulating the expression of Rb itself and CDKs, which phosphorylate Rb, and up-regulating the expression of the CDK inhibitor p21 through a p53-independent pathway. We also found that apoptosis was induced in a p53-dependent manner in PDCD4 knockdown HepG2 cells (p53+), although the mechanism of cell death in PDCD4 knockdown Hep3B cells (p53-) was different. Furthermore, PDCD4 knockdown induced cellular senescence characterized by β-galactosidase staining, and p21 knockdown rescued the senescence and cell death as well as the inhibition of Rb phosphorylation induced by PDCD4 knockdown. Thus, PDCD4 is an important cell cycle regulator of hepatoma cells and may be a promising therapeutic target for the treatment of hepatocellular carcinoma.
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PDCD4 knockdown stimulates CDKNI4 expression in TP53-deficient cells and siRNA-mediated TP53 knockdown cells, indicating that PDCD4 knockdown induces CDKNI4 expression in a TP53-independent manner.
“However, PDCD4 knockdown also stimulated CDKNI4 expression in TP53-deficient cells and siRNA-mediated TP53 knockdown cells, indicating that PDCD4 knockdown induces CDKNI4 expression in TP53-independent manner.”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [44]
The Results section, “PDCD4 Knockdown Up-Regulated the Expression of p21” (page unavailable), reports increased p21 in p53-deficient Hep3B cells and in cells with siRNA-mediated p53 knockdown, supporting the p53-independent finding. The paper identifies the induced inhibitor as p21, not CDKNI4; that gene designation is not supported by our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredsiRNA-mediated PDCD4 knockdown suppressed cell growth and induced senescence by inhibiting pRB phosphorylation via down-regulating pRB and CDKs and up-regulating p21(CDKNI4).
“We have observed that siRNA-mediated PDCD4 knockdown suppressed cell growth and induced senescence inhibiting retinoblastoma (RB)-protein (pRB)-phosphorylation via down-regulating the expression of pRB itself and cyclin dependent kinases (CDKs) which phosphorylate pRB and up-regulating the CDK inhibitor p21(CDKNI4) [44].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [44]
PDCD4 is an important cell cycle regulator and may contribute to control of the cell cycle via p21(CDKNI4) in hepatoma cells.
“The results indicate that PDCD4 is an important cell cycle regulator and may contribute to the control of cell cycle via p21(CDKNI4) in hepatoma cells.”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [44]
The role of PDCD4 in the RB-pathway might be different depending on the context and cell types.
“The results indicate that the role of PDCD4 in the RB-pathway might be different depending on the context and cell types.”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [44]
Modulation of CDK expression and cell death patterns induced by PDCD4 knockdown are different between wild type hepatoma HepG2 and mutant Hep3B cells, which are RB- and TP53-deficient.
“Guo et al demonstrated that the modulation of CDKs expression and cell death patterns induced by PDCD4 knockdown, are different between the wild type hepatoma HepG2 and the mutant Hep3B cells, which is RB- and TP53-defficient [44].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [44]
PDCD4 specific siRNA induces tumor cell death.
“PDCD4 specific siRNA also induces tumor cell death [43,44].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [44]
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Myofibrillar protein accumulation but reduced protein synthesis in PDCD4-depleted myotubes
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Zeng, Z., Shang, J., Chai, S., Ma, B., Han, X., Xu, Y., Wang, R., & Lv, Z. (2026) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-026-06243-9
Marín‐Maldonado, F., Santiago-Rosario, M. J., Fonseca‐Ferrer, W., Vlaar, C. P., Martínez‐Ferrer, M., Colón‐Sáez, J. O., & Duconge-Soler, J. (2026) · Frontiers in Aging · doi:10.3389/fragi.2026.1863781
- Authors
- Guo, J., Ozaki, I., Xia, J., Kuwashiro, T., Kojima, M., Takahashi, H., Ashida, K., Anzai, K., & Matsuhashi, S.
- Affiliations
- Saga University (JP)
- Corresponding author
- Ozaki, Iwata
- Venue
- Frontiers in Oncology
- Publisher
- Frontiers Media SA
- Published
- 2019-01-09
- Volume
- 8
- Pages
- 661-661
- ISSN
- 2234-943X (ISSN-L)
- PMC
- PMC6334536
- OpenAlex
- W2768317570
- Cited by
- 29
- References
- 75
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 4
- FWCI
- 1.36
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Oncology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- PDCD4, cellular senescence, hepatoma cells, p21, retinoblastoma protein phosphorylation, cyclin-dependent kinase inhibitors, p53-independent apoptosis, cell cycle regulation, hepatocellular carcinoma, tumor suppressor, therapeutic target
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