Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
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 ends...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
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...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...

You might also read

Related Articles

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

Sort by
Same author

Comprehensive proteogenomic characterization reveals clinically relevant molecular subtypes associated with medulloblastoma progression.

Experimental & molecular medicine·2026
Same author

Iron overload in steatotic hepatocytes drives systemic metabolic dysfunction via alterations in hepatokine production.

The Journal of clinical investigation·2026
Same author

[Analysis of Antimicrobial Resistance Trends and Characteristics of Vancomycin-resistant <i>Enterococcus faecium</i> Isolated in the Republic of Korea from 2018 to 2023].

Jugan geon-gang gwa jilbyeong·2025
Same author

Generation of orthotopic intracranial glioblastoma patient-derived xenograft models: insights into extrachromosomal DNA-driven MYC(N) and PDGFRA oncogene amplification and preliminary therapeutic evaluation.

Neoplasia (New York, N.Y.)·2025
Same author

MBNL2 enhances cisplatin resistance by regulating apoptosis in ovarian cancer cells.

BMB reports·2025
Same author

Fast and efficient method for parallel construction of targeted exome and methylome single-stranded DNA sequencing libraries.

Scientific reports·2025

Related Experiment Video

Updated: May 19, 2026

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
07:23

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome

Published on: June 15, 2016

A statin-regulated microRNA represses human c-Myc expression and function.

Apana A L Takwi1, Yan Li, Lindsey E Becker Buscaglia

  • 1Department of Biochemistry and Molecular Biology, School of Medicine, University of Louisville, KY, USA.

EMBO Molecular Medicine
|August 14, 2012
PubMed
Summary

Lovastatin upregulates miR-33b, a tumor suppressor microRNA, to inhibit c-Myc in medulloblastoma. This finding supports lovastatin as a potential therapy for c-Myc-driven cancers, using miR-33b as a biomarker.

More Related Videos

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
09:53

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge

Published on: June 15, 2018

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Related Experiment Videos

Last Updated: May 19, 2026

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
07:23

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome

Published on: June 15, 2016

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
09:53

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge

Published on: June 15, 2018

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • c-Myc dysregulation is a common hallmark of human cancers.
  • MicroRNAs (miRNAs) play a critical role in cancer development, with some regulating c-Myc.
  • The miR-33b gene, a primate-specific negative regulator of c-Myc, is located at 17p11.2, a locus often lost in medulloblastomas with c-Myc overproduction.

Purpose of the Study:

  • To identify novel regulators of c-Myc.
  • To investigate the therapeutic potential of targeting c-Myc dysregulation using drug repurposing and microRNAs as biomarkers.
  • To evaluate miR-33b as a negative regulator of c-Myc and its role in medulloblastoma.

Main Methods:

  • Screening of FDA-approved drugs for their effect on miR-33b expression.
  • Assessment of lovastatin's impact on cell proliferation, c-Myc expression, and function in medulloblastoma cells.
  • In vivo studies using orthotopic xenograft mouse models to evaluate lovastatin's efficacy in reducing tumor growth.

Main Results:

  • Lovastatin was identified to upregulate miR-33b expression.
  • Lovastatin treatment reduced cell proliferation and impaired c-Myc expression and function in miR-33b-positive medulloblastoma cells.
  • Low-dose lovastatin significantly reduced tumor growth in mice xenografted with miR-33b-positive cells, but not with miR-33b-negative cells.

Conclusions:

  • miR-33b acts as a primate-specific tumor suppressor by negatively regulating c-Myc.
  • Lovastatin demonstrates therapeutic potential for c-Myc-overexpressing cancers through miR-33b upregulation.
  • This study presents a promising drug repurposing strategy utilizing miR-33b as a predictive biomarker for cancer therapy.