Related Experiment Video

Updated: Jul 12, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

35.8K

RARγ promotes the invasion and metastasis of thyroid carcinoma by activating the JAK1-STAT3-CD24/MMPs axis

Fu-Xing Zhang1, Peng Xu2, Lin-Jun Zhang2

  • 1Xiamen Cell Therapy Research Center, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, Fujian Province, China; Department of General Surgery, The First Hospital Affiliated to Xiamen University, School of Medicine, Xiamen University, Xiamen, China.

International Immunopharmacology
|October 28, 2023
PubMed

Insights

Retinoic acid receptor gamma (RARγ) promotes thyroid carcinoma (TC) by increasing cell proliferation and invasion. Inhibiting RARγ may offer a new therapeutic strategy for treating this cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Nuclear receptors, including the retinoic acid receptor (RAR) superfamily, are implicated in tumor development.
  • The specific role and mechanism of RARγ in thyroid carcinoma (TC) remain unclear.

Purpose of the Study:

  • To investigate the function and mechanism of RARγ in thyroid carcinoma.
  • To determine if RARγ acts as a tumor promoter or suppressor in TC.

Main Methods:

  • Comparative analysis of RARγ expression in TC tissues and normal thyroid tissues.
  • Assessment of the correlation between RARγ expression and cancer cell phenotypes (proliferation, migration, invasion).
  • Investigation of the JAK1/STAT3 signaling pathway and CD24 expression following RARγ knockdown.
  • Evaluation of macrophage phagocytosis of TC cells in a coculture system, including the role of CD24-Siglec-10 interaction.

Main Results:

  • RARγ was significantly overexpressed in TC tissues compared to normal tissues.
  • RARγ expression correlated positively with increased cell proliferation, migration, and invasion.
  • RARγ knockdown reduced JAK1 and STAT3 phosphorylation, subsequently decreasing CD24 expression.
  • High membrane CD24 on TC cells facilitated escape from macrophage phagocytosis via Siglec-10, an effect reversed by CD24 antibody addition.

Conclusions:

  • RARγ promotes thyroid carcinoma development through a mechanism involving JAK1/STAT3 signaling and CD24-mediated immune evasion.
  • RARγ represents a potential therapeutic target for thyroid carcinoma.
Keywords:
CD24JAK1-STAT3 signalling pathwayMacrophagesMetastasisRARγThyroid carcinoma

More Related Videos

Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model09:03

Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model

Published on: October 16, 2017

8.8K
Lung Tumor Cell Recruitment Assay04:28

Lung Tumor Cell Recruitment Assay

Published on: February 26, 2019

5.4K

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
8.9K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.6K
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
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.6K
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
2.7K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.5K