Related Experiment Video

Updated: May 27, 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

Tumor suppressive microRNA-133a regulates novel molecular networks in lung squamous cell carcinoma

Yasumitsu Moriya1, Nijiro Nohata, Takashi Kinoshita

  • 1Department of General Thoracic Surgery, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chiba, Japan.

Journal of Human Genetics
|November 18, 2011
PubMed

Insights

MicroRNA 133a (miR-133a) acts as a tumor suppressor in lung squamous cell carcinoma (lung-SCC). Restoring miR-133a inhibits cancer cell proliferation by downregulating oncogenes ARPC5 and GSTP1.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Lung squamous cell carcinoma (lung-SCC) is a major subtype of lung cancer with complex molecular underpinnings.
  • MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
  • Reduced expression of miR-133a was observed in lung-SCC tissues compared to normal tissues.

Purpose of the Study:

  • To investigate the functional role of miR-133a in lung-SCC.
  • To identify novel cancer networks regulated by miR-133a in lung-SCC.
  • To explore the therapeutic potential of targeting miR-133a in lung-SCC.

Main Methods:

  • Analysis of miRNA expression in lung-SCC tissues and cell lines.
  • Restoration of miR-133a expression in lung-SCC cell lines (PC10, H157).
  • Genome-wide gene expression analysis to identify miR-133a targets.
  • Validation of target genes (ARPC5, GSTP1) using mRNA and protein level analysis and RNA interference (RNAi).

Main Results:

  • Restoration of miR-133a significantly inhibited lung-SCC cell proliferation, indicating a tumor-suppressive role.
  • Genome-wide analysis identified several candidate miR-133a targets, including ARPC5 and GSTP1.
  • ARPC5 and GSTP1 expression was elevated in lung-SCC clinical specimens.
  • miR-133a transfection repressed ARPC5 and GSTP1 at mRNA and protein levels.
  • RNAi knockdown of ARPC5 or GSTP1 significantly inhibited lung-SCC cell proliferation, suggesting their oncogenic function.

Conclusions:

  • miR-133a functions as a tumor suppressor in lung-SCC.
  • ARPC5 and GSTP1 are novel oncogenes in lung-SCC, regulated by miR-133a.
  • The miR-133a/ARPC5/GSTP1 pathway offers potential therapeutic targets for lung-SCC.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA (lncRNA)...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...