Related Experiment Video

Updated: Oct 23, 2025

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

14.0K

Clinical, genetic and pharmacological data support targeting the MEK5/ERK5 module in lung cancer

Adrián Sánchez-Fdez1,2,3, María Florencia Re-Louhau1,2, Pablo Rodríguez-Núñez1,2

  • 1Institute of Molecular and Cellular Biology of Cancer (IBMCC)-CSIC, Salamanca, Spain.

NPJ Precision Oncology
|August 18, 2021
PubMed

Insights

Targeting the MEK5/ERK5 pathway shows therapeutic promise for lung cancer. Inhibiting ERK5 slows tumor growth and enhances existing treatments, offering new hope for patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Lung cancer remains a leading cause of cancer-related death globally.
  • Understanding the molecular drivers of lung adenocarcinoma is crucial for developing novel therapies.
  • Previous research identified the MEK5/ERK5 mitogen-activated protein kinase (MAPK) pathway's role in lung tumor development.

Purpose of the Study:

  • To investigate the therapeutic potential of targeting the MEK5/ERK5 pathway in lung cancer.
  • To correlate MEK5/ERK5 levels with patient prognosis.
  • To evaluate the efficacy of genetic and pharmacological inhibition of MEK5/ERK5.

Main Methods:

  • Analysis of MEK5/ERK5 expression levels in lung cancer patient samples.
  • In vitro and in vivo studies using CRISPR/Cas9 to disrupt ERK5.
  • Pharmacological inhibition of the MEK5/ERK5 pathway.
  • Assessment of tumor growth inhibition and combination therapy effects.

Main Results:

  • Elevated MEK5/ERK5 levels are associated with a poorer prognosis in lung cancer patients.
  • Genetic disruption of ERK5 significantly inhibited lung cancer cell growth in vitro and in vivo.
  • Pharmacological targeting of the MEK5/ERK5 pathway demonstrated therapeutic efficacy.
  • ERK5 inhibition enhanced the anti-tumor effects of standard lung cancer treatments.

Conclusions:

  • The MEK5/ERK5 pathway is a viable therapeutic target for lung cancer.
  • Targeting MEK5/ERK5 offers a promising strategy to improve lung cancer treatment outcomes.
  • Combined approaches involving MEK5/ERK5 inhibition may overcome treatment resistance.

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

18.2K
Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure09:38

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

9.0K

Related Concept Videos

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...
7.2K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.0K
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...
4.0K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
5.3K
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...
5.8K
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...
4.7K