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Related Experiment Video

Updated: Aug 5, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Targeting Tumor Microenvironment Akt Signaling Represents a Potential Therapeutic Strategy for Aggressive Thyroid

Saied Mirshahidi^1,2, Isabella J Yuan³, Alfred Simental³

¹Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA.

International Journal of Molecular Sciences

|March 29, 2023

Summary

Tumor microenvironment stromal cells promote thyroid cancer progression by enhancing cancer stem-like cells via the PI3K/Akt pathway. Targeting Akt signaling offers a potential therapeutic strategy for aggressive thyroid cancer.

Keywords:

Akt signaling cancer stem cell targeting aggressive disease thyroid cancer tumor stromal cell

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Spontaneous Murine Model of Anaplastic Thyroid Cancer

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Published on: February 3, 2023

Area of Science:

Oncology
Cancer Biology
Molecular Medicine

Background:

The tumor microenvironment (TME) plays a critical role in cancer progression, yet its influence on thyroid cancer, particularly via stromal cells, remains understudied.
Understanding these interactions is crucial for developing novel therapeutic strategies for aggressive thyroid cancer.

Purpose of the Study:

To investigate the impact of TME stromal cells on cancer stem-like cells (CSCs) in thyroid cancer.
To elucidate the underlying molecular mechanisms, focusing on the PI3K/Akt pathway.
To evaluate the therapeutic potential of targeting this pathway in preclinical models and clinical samples.

Main Methods:

Utilized in vitro assays and xenograft models to study TME stromal cell effects on CSCs.
Investigated the role of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway.
Analyzed a clinical cohort of papillary thyroid carcinomas to correlate Akt signaling with lymph node metastasis.

Main Results:

TME stromal cells significantly enhance CSC self-renewal and invasiveness, primarily through the PI3K/Akt pathway.
Disrupting Akt signaling reduced CSC aggressiveness in vitro and suppressed tumor growth and metastasis in vivo.
Elevated Akt signaling in clinical samples correlated with lymph node metastasis in papillary thyroid carcinomas.

Conclusions:

TME stromal cells contribute to thyroid cancer progression by activating the PI3K/Akt pathway in CSCs.
Targeting Akt signaling within the TME presents a promising therapeutic avenue for aggressive thyroid cancer.
This approach demonstrated therapeutic benefits without significant alterations in tumor histology or stromal gene expression.