Related Experiment Video

Updated: Apr 24, 2026

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

7.1K

MicroRNA Deregulation in Anaplastic Thyroid Cancer Biology

Cesar Seigi Fuziwara1, Edna Teruko Kimura1

  • 1Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Avenida Professor Lineu Prestes 1524, Room 414, CEP, Butantã, 05508-000 São Paulo, SP, Brazil.

International Journal of Endocrinology
|September 10, 2014
PubMed

Insights

Anaplastic thyroid cancer (ATC) involves microRNA (miRNA) deregulation. Restoring tumor suppressor miRNAs or blocking oncogenic miRNAs offers a promising therapeutic strategy for this aggressive cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Anaplastic thyroid cancer (ATC) is a highly lethal, aggressive thyroid tumor resistant to conventional therapies.
  • Genetic alterations in TP53 and signaling pathways like MAPK and PI3K are common in ATC.
  • MicroRNAs (miRNAs), small non-coding RNAs regulating gene expression, are increasingly recognized for their roles in cancer.

Purpose of the Study:

  • To review the critical role of miRNA deregulation in anaplastic thyroid cancer (ATC) biology.
  • To highlight the implications of specific miRNA dysregulation in ATC pathogenesis and progression.
  • To explore the therapeutic potential of targeting miRNAs in ATC treatment.

Main Methods:

  • Literature review of studies investigating miRNA expression and function in thyroid cancer.
  • Analysis of miRNA deregulation patterns (upregulation and downregulation) in ATC.
  • Examination of the impact of specific miRNAs on key cellular processes like proliferation, invasion, and epithelial-to-mesenchymal transition (EMT).

Main Results:

  • Overexpression of certain miRNAs (e.g., miR-146b, miR-221, miR-222) is observed in ATC, contributing to tumorigenesis.
  • Downregulation of tumor suppressor miRNAs (e.g., miR-200 and miR-30 families) in ATC impairs regulation of cell migration, invasion, and EMT.
  • miRNA deregulation is a significant factor in the aggressive phenotype of anaplastic thyroid cancer.

Conclusions:

  • miRNA dysregulation is a key driver of anaplastic thyroid cancer (ATC) development and progression.
  • Targeting miRNA pathways, by restoring tumor suppressors or inhibiting oncogenic miRNAs, presents a promising therapeutic avenue for ATC.
  • Further research into miRNA-based therapies could significantly improve treatment efficacy for this deadly cancer.

More Related Videos

Spontaneous Murine Model of Anaplastic Thyroid Cancer05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

2.1K
An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

24.0K

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...
3.0K
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...
20.8K
MicroRNAs01:22

MicroRNAs

9.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
6.0K
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...
4.0K