Related Experiment Video

Updated: Sep 5, 2025

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

7.4K

Cdc42 promotes thyroid cancer cell proliferation and migration and tumor-associated macrophage polarization through

Deyi Huang1, Huali Qiu1, Lin Miao2

  • 1Ultrasound Department, The People's Hospital of Yuhuan, Yuhuan, China.

Journal of Biochemical and Molecular Toxicology
|July 13, 2022
PubMed

Insights

The study reveals that Cdc42 promotes thyroid cancer progression by enhancing cell migration and proliferation via the PTEN/AKT pathway. It also drives M2 macrophage polarization, suppressing T cell activity, suggesting Cdc42 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Cell Biology
  • Immunology

Background:

  • Thyroid cancer is a significant health concern.
  • Understanding the molecular mechanisms driving thyroid cancer progression is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role and mechanism of Cdc42 in thyroid cancer.
  • To explore Cdc42's impact on cell proliferation, migration, and the tumor microenvironment.

Main Methods:

  • Utilized knockdown and overexpression techniques for Cdc42 in thyroid cancer cell lines (WRO, TBP-3743).
  • Assessed cell migration, proliferation, PTEN nuclear translocation, lactic acid production, and macrophage polarization.
  • Conducted animal experiments to evaluate tumor growth and immune cell infiltration.

Main Results:

  • Cdc42 knockdown inhibited WRO cell migration and proliferation.
  • Cdc42 interacts with PTEN, hindering its nuclear translocation and activating the PTEN/AKT pathway.
  • Cdc42 overexpression increased lactic acid production, promoted M2 macrophage polarization, inhibited T cell function, and enhanced tumor growth in vivo.
  • Increased Treg and macrophage infiltration was observed in Cdc42-overexpressing tumors.

Conclusions:

  • Cdc42 promotes thyroid cancer cell proliferation and migration through the PTEN/AKT pathway.
  • Cdc42 facilitates M2 macrophage polarization and suppresses T cell activity via enhanced aerobic glycolysis.
  • Cdc42 serves as a potential diagnostic and prognostic biomarker and a therapeutic target for thyroid cancer.
Keywords:
Cdc42PTENlactatethyroid cancertumor-associated macrophage

More Related Videos

Induction and Analysis of Epithelial to Mesenchymal Transition10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

35.9K
Spontaneous Murine Model of Anaplastic Thyroid Cancer05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

1.7K

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...
3.9K
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...
3.9K
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...
6.6K
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...
4.6K
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...
6.4K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
5.7K