Induction of cell apoptosis in non-small cell lung cancer cells by cyclin A1 small interfering RNA

Related Experiment Video

Updated: Jul 19, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

Nam Hoon Cho1, Yoon Pyo Choi, Dong Suk Moon

  • 1Department of Pathology, Yonsei University College of Medicine, Seoul, Korea. cho1988@yumc.yonsei.ac.kr

Cancer Science
|September 21, 2006
PubMed

Insights

Targeting cyclin A1 and cyclin B1 with siRNA in lung cancer cells led to significant downregulation of key cell cycle proteins. This resulted in increased S phase fraction and apoptosis, suggesting cyclin A1 as a potential lung cancer therapy.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Cycle Regulation

Background:

  • Cyclin A1 and cyclin B1 are frequently overexpressed in tumors but minimally expressed in normal tissues.
  • Cyclin A1 expression is notably restricted to germ cells during meiosis.

Purpose of the Study:

  • To investigate the therapeutic potential of targeting cyclin A1 and cyclin B1 in lung cancer.
  • To explore the effects of siRNA-mediated knockdown of cyclin A1 and cyclin B1 on lung cancer cell lines.

Main Methods:

  • Utilized small interfering RNA (siRNA) to knock down cyclin A1 and cyclin B1 expression in H157 and H596 lung cancer cell lines.
  • Monitored the expression levels of cyclin B1, Cdc2, and CDK2 post-siRNA treatment.
  • Analyzed cell cycle progression and apoptosis pathways, including intrinsic and extrinsic apoptotic signaling.

Main Results:

  • siRNA-mediated knockdown of cyclin A1 resulted in significant downregulation of cyclin B1, Cdc2, and CDK2.
  • Observed a significant increase in the S phase fraction of treated lung cancer cells.
  • Induced apoptosis via modulation of intrinsic and extrinsic apoptotic pathways.

Conclusions:

  • Cyclin A1 and cyclin B1 knockdown significantly impacts cell cycle progression and induces apoptosis in lung cancer cells.
  • Cyclin A1 shows promise as a lung cancer-specific anticancer target.

More Related Videos

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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.