Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

MicroRNAs

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...

MicroRNAs

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...

MicroRNAs

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...

The Ras Gene

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...

Experimental RNAi

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...

MAPK Signaling Cascades

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Targeting the "undruggable": RNA-binding proteins in the spotlight in cancer therapy.

Seminars in cancer biology·2022

Same author

RNA-binding proteins: Underestimated contributors in tumorigenesis.

Seminars in cancer biology·2022

Same author

Insights into new mechanisms and models of cancer stem cell multidrug resistance.

Seminars in cancer biology·2019

Same author

Chondrocyte expansion is associated with loss of primary cilia and disrupted hedgehog signalling.

European cells & materials·2017

Same author

Absence of Relationship between Mitochondrial DNA Haplogroups and Cisplatin-Induced Hearing Loss.

International journal of otolaryngology·2017

Same author

The cancer stem-cell signaling network and resistance to therapy.

Cancer treatment reviews·2016

Search research articles

Related Experiment Video

Updated: Jun 16, 2026

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

Multiple microRNAs rescue from Ras-induced senescence by inhibiting p21(Waf1/Cip1).

V Borgdorff¹, M E Lleonart, C L Bishop

¹Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, London, UK.

|January 27, 2010

Summary

Oncogene-induced senescence (OIS) prevents cancer. Researchers identified specific microRNAs (miRNAs) that, when overexpressed, can block OIS by preventing the upregulation of the cell cycle inhibitor p21(Waf1/Cip1).

More Related Videos

The use of SC1 (Pluripotin) to Support mESC Self-renewal in the Absence of LIF

The use of SC1 (Pluripotin) to Support mESC Self-renewal in the Absence of LIF

Published on: November 18, 2009

Related Experiment Videos

Last Updated: Jun 16, 2026

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

The use of SC1 (Pluripotin) to Support mESC Self-renewal in the Absence of LIF

The use of SC1 (Pluripotin) to Support mESC Self-renewal in the Absence of LIF

Published on: November 18, 2009

Area of Science:

Cell Biology
Molecular Biology
Oncology

Background:

Oncogene-induced senescence (OIS) is a crucial tumor suppressive mechanism that halts proliferation upon oncogene activation.
Ras(G12V) oncogene expression in primary cells triggers OIS, acting as a safeguard against malignant transformation.
Understanding the molecular regulators of OIS is vital for cancer prevention strategies.

Purpose of the Study:

To identify key mediators, including microRNAs (miRNAs), that regulate oncogene-induced senescence (OIS).
To investigate the role of the cell cycle inhibitor p21(Waf1/Cip1) in OIS.
To discover novel miRNAs that can prevent Ras(G12V)-induced senescence.

Main Methods:

Genome-wide small interfering RNA (siRNA) and microRNA (miRNA) screening in human mammary epithelial cells (HMECs).
Assessing the effect of gene/miRNA knockdown or overexpression on Ras(G12V)-induced growth arrest.
Quantitative analysis of p21(Waf1/Cip1) expression levels.

Main Results:

siRNA-mediated knockdown of p21(Waf1/Cip1) rescued cells from Ras(G12V)-induced senescence.
A screen identified 28 miRNAs that prevented Ras(G12V)-induced growth arrest, including all members of the miR-106b family.
Overexpression of identified miRNAs, including miR-106b family members and similar sequences (miR-130b, miR-302 family, miR-512-3p, miR-515-3p), prevented Ras(G12V)-induced senescence by inhibiting p21(Waf1/Cip1) upregulation.

Conclusions:

The cell cycle inhibitor p21(Waf1/Cip1) plays a critical role in mediating OIS in human mammary epithelial cells.
Specific miRNAs, particularly the miR-106b family and related sequences, can modulate p21(Waf1/Cip1) activity and inhibit OIS.
These findings expand the known repertoire of miRNAs involved in tumor suppressor regulation and OIS.