Related Experiment Video

Updated: Oct 14, 2025

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

7.7K

MiR-499b-5p inhibits cervical cancer cell proliferation and induces apoptosis by targeting the Notch1 signaling

H-M Liu1, F Ji, Y Lu

  • 1Department of Gynaecology, First Affiliated Hospital, School of Medicine, Shihezi University, Xinjiang Uygur Autonomous Region, China. lhm5372j@163.com.

European Review for Medical and Pharmacological Sciences
|November 3, 2021
PubMed
Abstract

Insights

MicroRNA-499b-5p inhibits cervical cancer growth and promotes apoptosis by targeting the Notch1 pathway. This finding identifies miR-499b-5p as a potential therapeutic target for cervical cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cervical cancer remains a significant global health challenge.
  • Identifying novel molecular targets is crucial for effective treatment strategies.

Purpose of the Study:

  • To investigate the role of miR-499b-5p in cervical cancer.
  • To determine if miR-499b-5p targets the Notch1 signaling pathway.
  • To evaluate miR-499b-5p as a potential clinical target for cervical cancer.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) for gene expression analysis.
  • Cell viability (CCK-8), migration (Transwell), and apoptosis assays.
  • Dual-Luciferase reporter assay to confirm direct targeting.
  • In vivo xenograft models in nude mice.

Main Results:

  • MiR-499b-5p overexpression suppressed cervical cancer cell viability and migration while enhancing apoptosis.
  • MiR-499b-5p directly targets and inhibits Notch1 expression.
  • Notch1 knockdown mimicked the effects of miR-499b-5p.
  • Overexpression of miR-499b-5p reduced tumor growth in vivo.

Conclusions:

  • MiR-499b-5p acts as a tumor suppressor in cervical cancer.
  • The inhibitory effect is mediated through the Notch1 signaling pathway.
  • MiR-499b-5p holds promise as a novel therapeutic target for cervical cancer.

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

7.5K
Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

6.9K

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...
22.3K
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
4.6K
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...
5.0K
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...
7.0K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.1K
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...
4.7K