Related Experiment Video

Updated: Jan 7, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

597

GAB2 regulates lipid metabolism by activating the MEK/ERK/c-Myc pathway: impact on renal cell carcinoma progression

Weiqun Zhang1, Xianming Fei2, Pinqiong Qin1

  • 1Department of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.

European Journal of Medical Research
|December 24, 2025
PubMed
Abstract

Insights

Grb2-associated binding protein 2 (GAB2) promotes renal cell carcinoma (RCC) progression by enhancing lipid accumulation via the MEK/ERK/c-Myc pathway. Targeting GAB2 may offer a new strategy for RCC management.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Grb2-associated binding protein 2 (GAB2) is a cytoplasmic scaffold protein implicated in various cancers.
  • Its specific role and mechanisms in renal cell carcinoma (RCC) development are not well understood.

Purpose of the Study:

  • To investigate the role and underlying mechanisms of GAB2 in the progression of renal cell carcinoma (RCC).

Main Methods:

  • Examined GAB2 mRNA levels in normal renal cells and RCC cell lines.
  • Assessed the impact of GAB2 knockdown and overexpression on RCC cell proliferation, apoptosis, migration, and lipid metabolism.
  • Evaluated the MEK/ERK/c-Myc pathway activation and tumor growth in vivo using a xenograft mouse model and a MEK inhibitor (U0126).

Main Results:

  • GAB2 expression was significantly higher in RCC cells compared to normal cells.
  • GAB2 knockdown inhibited RCC cell viability, migration, and lipid accumulation, while inducing apoptosis.
  • GAB2 overexpression promoted tumor growth, lipid synthesis, and activated the MEK/ERK/c-Myc pathway, effects partially reversed by U0126.

Conclusions:

  • GAB2 promotes RCC progression by activating the MEK/ERK/c-Myc pathway, leading to increased lipid accumulation.
  • GAB2 represents a potential therapeutic target for managing renal cell carcinoma.
Keywords:
GAB2Lipid metabolismMEK/ERK/c-Myc pathwayRenal cell carcinomaTumor development

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

18.5K
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

14.1K

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...
4.6K
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...
7.8K
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
7.6K
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...
5.2K
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...
7.7K
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...
5.0K