Related Experiment Video

Updated: May 9, 2025

Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line
06:38

Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line

Published on: August 2, 2021

26.5K

Overexpression of FMOD in Thyroid Carcinoma Triggers M1-Like Tumor-Associated Macrophage Polarization by Targeting

Xiangnan Fang1, Xuemei Huang2, Wenfeng Liu2

  • 1Department of Endocrinology and Metabolism, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 29, 2025
PubMed

Insights

Fibromodulin (FMOD) acts as a tumor suppressor in thyroid carcinoma. Overexpressing FMOD inhibits cancer growth, promotes apoptosis, and enhances anti-tumor immunity by modulating macrophages and targeting Rap1B.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Thyroid carcinoma presents limited treatment options, necessitating the identification of novel therapeutic targets.
  • Fibromodulin (FMOD) has been implicated in various cancers, but its role in thyroid carcinoma remains unclear.

Purpose of the Study:

  • To investigate the function of FMOD as a potential therapeutic target in thyroid carcinoma.
  • To elucidate the underlying mechanisms of FMOD's action, including its effects on tumor cells, macrophages, and downstream signaling pathways.

Main Methods:

  • Bioinformatic analysis to identify candidate therapeutic targets, followed by experimental validation of FMOD.
  • In vitro assays (cell counting kit-8, wound healing, Transwell, flow cytometry) to assess FMOD's impact on thyroid carcinoma cell behavior.
  • In vivo studies using nude mice to monitor tumor growth, and co-culture experiments to analyze tumor-associated macrophage (TAM) polarization and Rap1B signaling.

Main Results:

  • FMOD was identified as a tumor suppressor gene in thyroid carcinoma.
  • FMOD overexpression inhibited cell viability, migration, and invasion, while promoting apoptosis in thyroid carcinoma cells.
  • In vivo, FMOD upregulation suppressed tumor growth and promoted M1-like TAM polarization, partly through downregulation of Ras-association proximate 1B (Rap1B).

Conclusions:

  • FMOD demonstrates significant inhibitory effects on thyroid carcinoma progression.
  • The tumor-suppressive role of FMOD is mediated by enhancing M1-like TAM polarization via the Rap1B signaling pathway.
  • FMOD represents a promising therapeutic target for thyroid carcinoma treatment.
Keywords:
FMODM1‐like polarizationRap1Bthyroid carcinomatumor‐associated macrophages

More Related Videos

Reprograming Model of Human Monocyte-derived Macrophages for In-vitro Assays08:37

Reprograming Model of Human Monocyte-derived Macrophages for In-vitro Assays

Published on: April 18, 2025

91
Time-Lapse 2D Imaging of Phagocytic Activity in M1 Macrophage-4T1 Mouse Mammary Carcinoma Cells in Co-cultures10:23

Time-Lapse 2D Imaging of Phagocytic Activity in M1 Macrophage-4T1 Mouse Mammary Carcinoma Cells in Co-cultures

Published on: December 14, 2019

9.0K

Related Concept Videos

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...
3.6K
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...
3.3K
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...
4.3K
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...
4.9K
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...
6.3K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.1K