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mTOR Signaling and Cancer Progression

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.
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Related Experiment Video

Updated: Dec 23, 2025

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

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

Published on: June 26, 2019

Afatinib is active in osteosarcoma in osteosarcoma cell lines.

Marlid Cruz-Ramos^1,2, Yessica Zamudio-Cuevas³, Daniel Medina-Luna^3,4

¹Oncology Translational Laboratory, Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain. marlid.cruz@gmail.com.

Journal of Cancer Research and Clinical Oncology

|April 26, 2020

Summary

Afatinib, an ErbB family blocker, demonstrated significant antitumor effects in osteosarcoma cell lines by reducing cell viability, motility, and migration. This study highlights afatinib

Keywords:

Afatinib Antitumoral ErbB Osteosarcoma

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Area of Science:

Oncology
Molecular Biology
Pharmacology

Background:

Osteosarcoma is a prevalent bone tumor in adolescents and young adults.
Metastatic osteosarcoma has poor prognosis, necessitating novel therapeutic strategies.
Aberrations in the ErbB pathway are implicated in osteosarcoma development.

Purpose of the Study:

To investigate the anti-cancer effects of afatinib, an ErbB family blocker, on osteosarcoma cell lines.
To evaluate afatinib's impact on osteosarcoma cell viability, motility, and migration.
To assess afatinib's modulation of the ErbB signaling pathway in osteosarcoma.

Main Methods:

Cell viability assays were performed on human osteosarcoma cell lines treated with varying concentrations of afatinib.
Wound-healing and Transwell chamber assays were used to measure cell motility and invasion.
Western blot analysis was employed to monitor ErbB pathway modulation by afatinib.

Main Results:

Afatinib treatment led to significant inhibition of cell viability in osteosarcoma cell lines.
A reduction in the motility and migration capacity of osteosarcoma cells was observed.
Afatinib decreased the phosphorylation of key signaling components within the ErbB pathway in the HOS cell line.

Conclusions:

Afatinib exhibits a notable antitumor effect against multiple osteosarcoma cell lines.
The drug significantly impacts osteosarcoma cell viability, motility, and migration.
Afatinib effectively reduces ErbB pathway activity, suggesting its therapeutic potential in osteosarcoma.