Related Experiment Video
Updated: Jan 22, 2026

Anticancer Efficacy of Photodynamic Therapy with Lung Cancer-Targeted Nanoparticles
Published on: December 1, 2016
Targeting mTOR for cancer therapy
Hui Hua1, Qingbin Kong2, Hongying Zhang2
1State Key Laboratory of Biotherapy, Laboratory of Stem Cell Biology, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, 610041, China.
Abstract:
Mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. mTOR is usually assembled into several complexes such as mTOR complex 1/2 (mTORC1/2). In cooperation with raptor, rictor, LST8, and mSin1, key components in mTORC1 or mTORC2, mTOR catalyzes the phosphorylation of multiple targets such as ribosomal protein S6 kinase β-1 (S6K1), eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), Akt, protein kinase C (PKC), and type-I insulin-like growth factor receptor (IGF-IR), thereby regulating protein synthesis, nutrients metabolism, growth factor signaling, cell growth, and migration. Activation of mTOR promotes tumor growth and metastasis. Many mTOR inhibitors have been developed to treat cancer. While some of the mTOR inhibitors have been approved to treat human cancer, more mTOR inhibitors are being evaluated in clinical trials. Here, we update recent advances in exploring mTOR signaling and the development of mTOR inhibitors for cancer therapy. In addition, we discuss the mechanisms underlying the resistance to mTOR inhibitors in cancer cells.
Insights
Mechanistic target of rapamycin (mTOR) signaling regulates cell growth and is crucial in cancer. This review covers mTOR inhibitors for cancer therapy and discusses resistance mechanisms.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- Mechanistic target of rapamycin (mTOR) is a key protein kinase regulating fundamental cellular processes like growth, metabolism, and immunity.
- mTOR functions within complexes (mTORC1/2) and phosphorylates numerous targets, influencing protein synthesis, nutrient metabolism, and growth factor signaling.
- Aberrant mTOR activation is implicated in promoting tumor growth and metastasis, making it a significant target in cancer research.
Purpose of the Study:
- To provide an updated review of recent advances in understanding mTOR signaling pathways.
- To summarize the development of mTOR inhibitors for cancer therapy.
- To discuss the mechanisms of resistance to mTOR inhibitors in cancer cells.
Main Methods:
- Literature review of recent scientific publications on mTOR signaling and cancer therapy.
- Analysis of the roles of mTOR complexes and their targets in cellular regulation.
- Synthesis of information on approved and investigational mTOR inhibitors.
Main Results:
- mTOR signaling is critical for cell growth, survival, metabolism, and immunity, with dysregulation driving cancer progression.
- Numerous mTOR inhibitors have been developed, with some approved for clinical use, while others are in ongoing trials.
- Understanding resistance mechanisms is crucial for optimizing mTOR-targeted cancer therapies.
Conclusions:
- mTOR signaling is a vital regulator of cellular functions and a significant driver of cancer.
- mTOR inhibitors represent a promising therapeutic strategy for various cancers.
- Further research into resistance mechanisms is essential for improving the efficacy of mTOR-targeted treatments.
More Related Videos
Related Concept Videos
Targeted Cancer Therapies
There are several types of targeted therapies against...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Cancer Therapies
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
PI3K/mTOR/AKT Signaling Pathway
Gene Therapy
Group Therapy

