Related Experiment Video

Updated: Jul 10, 2025

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
09:38

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

8.9K

MYC expression and fatty acid oxidation in EGFR-TKI acquired resistance

GuoSheng Wang1, Tao Li2, Yuan Wan3

  • 1Department of Pulmonary and Critical Care Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China; The Pq Laboratory of Micro/Nano BiomeDx, Department of Biomedical Engineering, Binghamton University-SUNY, Binghamton, NY 13902, United States.

Drug Resistance Updates : Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy
|November 20, 2023
PubMed

Insights

This study reveals an inverse link between MYC expression and immune cell function in EGFR-TKI resistance. Impaired MYC and fatty acid oxidation in T cells suggest caution with MYC inhibitors.

Area of Science:

  • Oncology
  • Immunology
  • Metabolism

Background:

  • Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors (EGFR-TKIs) are crucial in cancer therapy.
  • Acquired resistance to EGFR-TKIs remains a significant clinical challenge.
  • The role of MYC oncogene and immune cell metabolism in resistance is not fully understood.

Purpose of the Study:

  • To investigate the correlation between MYC expression and immune cell function during EGFR-TKI resistance.
  • To explore the metabolic status of T cells in the context of acquired resistance.
  • To assess the potential of targeting MYC for overcoming TKI resistance.

Main Methods:

  • Analysis of MYC expression in tumor and immune cells from patients with EGFR-TKI resistance.
  • Assessment of fatty acid oxidation (FAO) metabolism in tissue-resident memory (TRM) CD8+ T cells.
  • Correlation studies between MYC levels, immune cell function, and TKI response.

Main Results:

  • A unique inverse correlation was identified between MYC expression in tumor cells and immune cells.
  • Significantly impaired MYC expression and FAO metabolism were observed in TRM CD8+ T cells.
  • These alterations in immune cell metabolism are linked to the development of EGFR-TKI resistance.

Conclusions:

  • MYC dysregulation and impaired T cell metabolism are implicated in EGFR-TKI resistance mechanisms.
  • Findings suggest that immune factors must be considered when evaluating MYC inhibitors for TKI resistance.
  • Further research is needed to validate these preliminary findings and explore therapeutic strategies.
Keywords:
EGFR-TKI resistanceFatty acid metabolismLung cancerMYCT cell

More Related Videos

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib09:38

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Published on: June 26, 2019

8.0K
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

18.0K

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...
6.5K
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...
3.8K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.3K
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...
3.6K
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...
4.5K