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N-linoleyltyrosine resisted the growth of non-small cell lung cancer cells via the regulation of CB1 and CB2 involvement of PI3K and ERK pathways
Ist Teil von
Frontiers in pharmacology, 2023-06, Vol.14, p.1164367-1164367
Ort / Verlag
Frontiers Media S.A
Erscheinungsjahr
2023
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
Background:
N-linoleyltyrosine (NITyr), one of the anandamide analogs, exerts activity via the endocannabinoid receptors (CB
1
and CB
2
), which showed anti-tumor effects in various tumors. Therefore, we speculated that NITyr might show anti-non-small cell lung cancer (NSCLC) effects via the CB
1
or CB
2
receptor. The purpose of the investigation was to reveal the anti-tumor ability of NITyr on A549 cells and its mechanisms.
Methods:
The viability of A549 cells was measured by MTT assay, and the cell cycle and apoptosis were both examined by flow cytometry; in addition, cell migration was tested by wound healing assay. Apoptosis-related markers were measured by immunofluorescence. The downstream signaling pathways (PI3K, ERK, and JNK) of CB
1
or CB
2
were examined through Western blotting. The expressions of CB
1
and CB
2
were detected by immunofluorescence. Finally, the AutoDock software was used to validate the binding affinity between the targets, such as CB
1
and CB
2,
with NITyr.
Results:
We found that NITyr inhibited cell viability, hindered the cell cycle, resulted in apoptosis, and inhibited migration. The CB
1
inhibitor, AM251, and the CB
2
inhibitor, AM630, weakened the aforementioned phenomenon. The immunofluorescence assay suggested that NITyr upregulated the expression of CB
1
and CB
2
. Western blot analysis indicated that NITyr upregulated the expression of p-ERK, downregulated the expression of p-PI3K, and did not affect p-JNK expression. In conclusion, NITyr showed a role in inhibiting NSCLC through the activation of CB
1
and CB
2
receptors involved in PI3K and ERK pathways.