Related Experiment Video

Updated: Feb 22, 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

7.8K

Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

Maria Chiara Anania1, Elena Cetti1, Daniele Lecis1

  • 1Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Cancer Letters
|September 28, 2017
PubMed

Insights

Targeting the COPZ1 gene, crucial for thyroid tumor cell survival, offers a novel therapeutic strategy. Depleting COPZ1 induces cancer cell death and reduces tumor growth, paving the way for new thyroid cancer treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Thyroid carcinoma often has a good prognosis, but aggressive forms lack effective treatments.
  • Identifying novel therapeutic targets is crucial for advanced thyroid cancer.
  • The non-oncogene addiction paradigm seeks genes essential for cancer cells but not normal cells.

Purpose of the Study:

  • To investigate the mechanisms by which coatomer protein complex ζ1 (COPZ1) depletion induces thyroid tumor cell death.
  • To evaluate COPZ1 as a potential therapeutic target for thyroid cancer.

Main Methods:

  • siRNA-mediated functional screening to identify essential genes in thyroid tumor cells.
  • siRNA-mediated COPZ1 depletion in cell cultures and mouse xenografts.
  • Analysis of cellular processes including autophagy, endoplasmic reticulum stress, unfolded protein response, and apoptosis.

Main Results:

  • COPZ1 depletion triggers abortive autophagy, endoplasmic reticulum stress, unfolded protein response, and apoptosis in thyroid tumor cells.
  • siRNA targeting COPZ1 significantly reduced tumor growth in mouse xenografts.
  • COPZ1 is essential for the viability of thyroid tumor cells.

Conclusions:

  • COPZ1 plays a critical role in thyroid tumor cell viability.
  • COPZ1 represents a promising therapeutic target for novel thyroid cancer treatments.
Keywords:
COPZ1Cell deathNon-oncogene addictionThyroid carcinoma

More Related Videos

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.8K
An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

21.7K

Related Concept Videos

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...
9.0K
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...
8.2K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
6.1K
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
30
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...
6.1K
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...
5.3K