Bibliographic Details
| Title: |
Implication of mTOR Signaling in NSCLC: Mechanisms and Therapeutic Perspectives |
| Authors: |
Antonios N. Gargalionis, Kostas A. Papavassiliou, Athanasios G. Papavassiliou |
| Source: |
Cells, Vol 12, Iss 15, p 2014 (2023) |
| Publisher Information: |
MDPI AG, 2023. |
| Publication Year: |
2023 |
| Collection: |
LCC:Cytology |
| Subject Terms: |
mTOR signaling, non-small cell lung cancer (NSCLC), PI3K, Akt, rapamycin, Cytology, QH573-671 |
| More Details: |
Mechanistic target of the rapamycin (mTOR) signaling pathway represents a central cellular kinase that controls cell survival and metabolism. Increased mTOR activation, along with upregulation of respective upstream and downstream signaling components, have been established as oncogenic features in cancer cells in various tumor types. Nevertheless, mTOR pathway therapeutic targeting has been proven to be quite challenging in various clinical settings. Non-small cell lung cancer (NSCLC) is a frequent type of solid tumor in both genders, where aberrant regulation of the mTOR pathway contributes to the development of oncogenesis, apoptosis resistance, angiogenesis, cancer progression, and metastasis. In this context, the outcome of mTOR pathway targeting in clinical trials still demonstrates unsatisfactory results. Herewith, we discuss recent findings regarding the mechanisms and therapeutic targeting of mTOR signaling networks in NSCLC, as well as future perspectives for the efficient application of treatments against mTOR and related protein molecules. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2073-4409 |
| Relation: |
https://www.mdpi.com/2073-4409/12/15/2014; https://doaj.org/toc/2073-4409 |
| DOI: |
10.3390/cells12152014 |
| Access URL: |
https://doaj.org/article/4193893509f64b47955ad33c9605383b |
| Accession Number: |
edsdoj.4193893509f64b47955ad33c9605383b |
| Database: |
Directory of Open Access Journals |
|
Full text is not displayed to guests. |
Login for full access.
|
