Related Experiment Video

Updated: Nov 18, 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

7.6K

GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling

Saifei He1, Miao Zhang1, Ying Ye1

  • 1Central Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200137, P.R. China.

Molecular Medicine Reports
|February 4, 2021
PubMed

Insights

GINS2 protein plays a key role in thyroid cancer (TC) progression by affecting cell viability, migration, and invasion. Silencing GINS2 inhibits tumor growth and induces apoptosis, suggesting it as a potential therapeutic target for TC.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Thyroid cancer (TC) is the most common endocrine malignancy globally.
  • GINS complex subunit 2 (GINS2) is implicated in cellular processes like migration, invasion, and growth.
  • Understanding GINS2's role in TC is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the mechanisms by which GINS2 influences cell viability, migration, and invasion in thyroid cancer cells.
  • To explore the potential of GINS2 as a therapeutic target for thyroid cancer treatment.

Main Methods:

  • Cell viability was assessed using MTT assays.
  • Cell migration and invasion were evaluated through wound healing and Transwell assays.
  • Protein expression and apoptosis were analyzed using Western blotting and immunofluorescence, respectively.

Main Results:

  • GINS2 interference significantly reduced cell viability, migration, and invasion in TC cell lines (K1 and SW579).
  • GINS2 silencing induced apoptosis in thyroid cancer cells.
  • GINS2 inhibition suppressed key proteins in the Mitogen-Activated Protein Kinase (MAPK) signaling pathway, including JNK, ERK, and p38.

Conclusions:

  • GINS2 plays a critical role in thyroid cancer cell viability, migration, and invasion.
  • GINS2 regulates the MAPK signaling pathway, suggesting its involvement in TC progression.
  • GINS2 represents a potential therapeutic target for managing thyroid cancer.
Keywords:
GINS complex subunit 2thyroid cancercell viabilitymigration and invasionMAPK signaling pathway

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

36.2K
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.8K

Related Concept Videos

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...
6.9K
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...
4.1K
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...
7.2K
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...
7.4K
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...
4.7K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.3K