Related Experiment Video

Updated: Jul 26, 2025

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

1.7K

KAT5 Inhibitor NU9056 Suppresses Anaplastic Thyroid Carcinoma Progression through c-Myc/miR-202 Pathway

Wenjing Xu1,2,3, Liwei Xie1,2,3, Yingying Yang1,2,3

  • 1Department of Radiotherapy and Oncology, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China.

International Journal of Endocrinology
|June 21, 2023
PubMed
Abstract

Insights

The KAT5 inhibitor NU9056 suppresses anaplastic thyroid carcinoma (ATC) by targeting KAT5, downregulating miR-202, and inhibiting cell growth. This highlights KAT5 as a potential therapeutic target for aggressive ATC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Anaplastic thyroid carcinoma (ATC) is an aggressive cancer with poor prognosis.
  • Elevated lysine acetyltransferase 5 (KAT5) expression is linked to poorer outcomes in ATC patients.

Purpose of the Study:

  • To investigate the therapeutic potential of the KAT5 inhibitor NU9056 in human ATC cells.
  • To elucidate the molecular mechanisms underlying NU9056's effects on ATC.

Main Methods:

  • Analysis of TCGA dataset for KAT5 expression and patient outcomes.
  • In vitro and in vivo studies of NU9056 on normal and ATC cells.
  • MicroRNA sequencing, qPCR, and dual-luciferase reporter assays to identify downstream targets.

Main Results:

  • NU9056 suppressed ATC cell survival, growth, migration, invasion, and tube formation, while enhancing radiosensitivity and chemosensitivity.
  • NU9056 treatment led to decreased miR-202-5p levels, which were linked to c-Myc regulation.
  • NU9056 inhibited ATC proliferation in vivo by targeting KAT5 and reducing c-Myc half-life.

Conclusions:

  • NU9056 effectively targets KAT5, leading to c-Myc downregulation, reduced miR-202 expression, and suppression of ATC.
  • KAT5 inhibition represents a promising therapeutic strategy for anaplastic thyroid carcinoma.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice00:07

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.4K
An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

21.2K

Related Concept Videos

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...
4.8K
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...
3.8K
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...
4.6K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.7K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
2.9K
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.4K