Review of 46 terpenoids affecting autophagy and senescence in lung cancer cells
This review summarizes preclinical reports that 46 structurally diverse terpenoids and analogs affect both autophagy and cellular senescence in lung cancer cells, often via shared signaling nodes; clinical use is limited by poor solubility, low bioavailability and delivery challenges. [1]
Automatic summary · not editorially reviewed
The key findings
Preclinical studies report that terpenoids affect autophagy and cellular senescence, which have both tumor-suppressive and tumor-progressive effects. [1]
The review summarizes effects of 46 structurally diverse terpenoids and their analogs on autophagy and cellular senescence in pulmonary cancer cells. [1]
Clinical translation of terpenoids is limited by poor solubility, low bioavailability and challenges in targeted delivery. [1]
The source at a glance
- Study type / format
- Review of preclinical studies (abstract only)
- Population / context
- Pulmonary cancer cells in preclinical studies; patients with lung cancer are mentioned only as the broader disease context.
- Summary based on
- Study abstract
- Original publication
- September 11, 2026
Terpenoids and two cell pathways in lung cancer
Lung cancer is among the top causes of cancer death worldwide, and current therapies achieve little success because of late diagnoses, resistance and side effects. Terpenoids are secondary metabolites produced by plants and have been extensively investigated for anticancer activity. Preclinical studies report that they affect autophagy and cellular senescence, two mechanisms with both tumor-suppressive and tumor-progressive effects.
Supporting source [1]
46 terpenoids and shared signaling nodes
The review summarizes effects of 46 structurally diverse terpenoids, including monoterpenoids, diterpenoids, triterpenoids, sesquiterpenoids and their analogs, on autophagy and cellular senescence in pulmonary cancer cells. Most of these agents were reported to affect both pathways by targeting central signaling nodes such as AMPK, NF-κB, MAPK/ERK/JNK, PI3K/AKT/mTOR, reactive oxygen species, p53, Rb, cell cycle arrest and senescence-associated secretory phenotype factors.
Supporting source [1]
Preclinical promise versus clinical translation limits
The review highlighted that autophagy and cellular senescence can be exploited in lung cancer treatment to provide improved benefit to patients. Although preclinical studies provide promising evidence for the anticancer potential of terpenoids, their clinical translation is limited by poor solubility, low bioavailability and challenges in targeted delivery.
Supporting source [1]
How to interpret this
This is an abstract only; the full text was not reviewed. It describes a review of preclinical studies in pulmonary cancer cells, not human trials, and reports no clinical outcomes. The abstract does not specify study designs, sample sizes or effect sizes of the summarized studies. Statements about exploiting autophagy and senescence are proposals, not validated treatments.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Niharika K, Muthuvenugopal N, Das M, Kiruthiga C. · europepmc.org · September 11, 2026