Related Experiment Video
Updated: May 20, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Runx2 isoform I controls a panel of proinvasive genes driving aggressiveness of papillary thyroid carcinomas
Valentina Sancisi1, Gloria Borettini, Sally Maramotti
1Laboratory of Molecular Biology, Department of Oncology, Azienda Ospedaliera Arcispedale S. Maria Nuova, Istituto di Ricovero e Cura a Carattere Scientifico, viale Risorgimento 80, 42123 Reggio Emilia, Italy.
Context:
The ability of tumor cells to invade adjacent tissues is governed by a complicated network of molecular signals, most of which have not yet been identified. In a recent work, we reported that the transcriptional regulator Id1 contributes to thyroid cancer progression by powering the invasion capacity of tumor cells.
Objective:
The intent of this work was to further investigate the biology of invasive thyroid tumors, through the analysis of the molecular interactions existing between Id1 and some of its target genes and through the characterization of the function of these factors in the progression of thyroid tumors.
Results:
We showed that Id1 controls the expression of the Runx2 isoform I and that this transcription factor plays a central role in mediating the Id1 proinvasive function in thyroid tumor cells. We demonstrated that Runx2 regulates proliferation, migration, and invasiveness by activating a panel of genes involved in matrix degradation and cellular invasion, which we previously identified as Id1 target genes in thyroid tumor cells. Finally, we show that Runx2 is strongly expressed in metastatic human thyroid tumors both at the primary site and in metastases.
Conclusion:
Overall, our experiments demonstrate the existence of a previously unknown molecular axis that controls thyroid tumor invasiveness by altering the ability of tumor cells to interact with the surrounding microenvironment. These factors could prove to be valuable markers that permit early diagnosis of aggressive thyroid tumors.
Insights
The transcriptional regulator Id1 promotes thyroid cancer invasion by controlling Runx2 expression. This axis impacts tumor cell interaction with the microenvironment, offering potential diagnostic markers for aggressive thyroid tumors.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Tumor cell invasion is regulated by complex molecular signals, many unidentified.
- The transcriptional regulator Id1 was previously shown to enhance thyroid cancer cell invasion.
Purpose of the Study:
- Investigate the molecular interactions between Id1 and its target genes in invasive thyroid tumors.
- Characterize the role of these factors in thyroid tumor progression.
Main Methods:
- Analysis of molecular interactions between Id1 and target genes.
- Functional characterization of identified factors in thyroid tumor cells.
- Expression analysis of Runx2 in human thyroid tumors.
Main Results:
- Id1 controls the expression of the Runx2 isoform I, which mediates Id1's proinvasive function.
- Runx2 activates genes involved in matrix degradation and cellular invasion, crucial for tumor progression.
- Runx2 is highly expressed in metastatic human thyroid tumors.
Conclusions:
- A novel molecular axis involving Id1 and Runx2 controls thyroid tumor invasiveness.
- This axis alters tumor cell interaction with the surrounding microenvironment.
- These factors may serve as valuable early diagnostic markers for aggressive thyroid tumors.
Related Concept Videos
Inheritance of Chromatin Structures
Abnormal Proliferation
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Non-LTR Retrotransposons
PI3K/mTOR/AKT Signaling Pathway
