Related Experiment Video

Updated: May 16, 2026

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
07:26

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

Silencing P12CDK²AP¹ with a lentivirus promotes HaCaT cell proliferation

Moyi Sun1, Jun Zheng, Hui Xue

  • 1Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China. moyisun@163.com

Molecular Medicine Reports
|December 12, 2012
PubMed

Insights

The tumor suppressor P12CDK2AP1, downregulated in head and neck cancers, was knocked down using lentivirus-mediated shRNA in skin cells. This knockdown significantly increased cell proliferation, suggesting a role in cancer development.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • P12CDK2AP1 acts as a tumor suppressor by inhibiting cyclin-dependent kinase 2 (CDK2) and DNA replication.
  • Downregulation of P12CDK2AP1 is observed in head and neck squamous cell carcinomas (HNSCCs).
  • Gene silencing using RNA interference (RNAi) is a key method for functional gene analysis.

Purpose of the Study:

  • To investigate the functional role of P12CDK2AP1 in head and neck squamous cell carcinomas (HNSCCs).
  • To assess the efficacy of lentivirus-mediated short hairpin RNA (shRNA) for P12CDK2AP1 knockdown in normal human skin keratinocytes (HaCaT).

Main Methods:

  • Utilized lentivirus-mediated shRNA for targeted gene knockdown.
  • Employed RNA interference (RNAi) to reduce endogenous P12CDK2AP1 expression in HaCaT cells.
  • Assessed the impact of P12CDK2AP1 knockdown on HaCaT cell proliferation in vitro.

Main Results:

  • Lentivirus-mediated RNA interference effectively reduced P12CDK2AP1 expression in HaCaT cells.
  • Significant promotion of HaCaT cell proliferation was observed following P12CDK2AP1 knockdown.
  • Demonstrated the potential of lentiviral vectors for gene knockdown and functional studies.

Conclusions:

  • P12CDK2AP1 knockdown promotes keratinocyte proliferation, suggesting its tumor-suppressive role in HNSCC.
  • Lentivirus-mediated RNAi is an effective tool for studying gene function in keratinocytes.
  • Lentiviral vectors show potential for therapeutic applications in siRNA delivery for HNSCC treatment.

More Related Videos

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Study of Dendritic Cell Development by Short Hairpin RNA-Mediated Gene Knockdown in a Hematopoietic Stem and Progenitor Cell Line In vitro06:12

Study of Dendritic Cell Development by Short Hairpin RNA-Mediated Gene Knockdown in a Hematopoietic Stem and Progenitor Cell Line In vitro

Published on: March 7, 2022

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...