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Current Molecular Medicine


ISSN (Print): 1566-5240
ISSN (Online): 1875-5666

Research Article

Apigenin Inhibits Proliferation, Migration, and Invasion of Human Tongue Carcinoma Tca8113 Cells Through Regulating the MAPK Signaling Pathways

Author(s): Yun-Ze Xuan, Li-Zhi Xu, Cheng-Ri Jin and Kang-Juan Yang*

Volume 21 , Issue 8 , 2021

Published on: 22 October, 2020

Page: [690 - 697] Pages: 8

DOI: 10.2174/1566524020666201022120420

Price: $65


Objective: This study aimed to examine the effects of apigenin (API) on the proliferation, migration, and invasion of human tongue squamous cell carcinoma Tca8113 cells and explore its probable mechanisms.

Methods: After treating Tca8113 cells with API, the cell proliferation, migration, and invasive capacities were identified by tetrazolium salt colorimetry (MTT) assay, cell scratch test, and Transwell chamber test. Cellular immunofluorescence staining was used to localize mitogen-activated protein kinase 1 (MAPK1) and extracellular regulated protein kinase (ERK) 1/2 proteins. Western blot was used to detect the variations of the related protein expression levels.

Results:① Through the MTT assay, API significantly inhibited cell proliferation (P<0.01). ②In the cell scratch test, the distance of lateral migration after the API treatment was significantly shorter compared to the control group (P<0.01). ③The invasion rate in the lower chamber of the Transwell chamber was lower in the API group (P<0.01). ④ Cellular immunofluorescence staining presented that the total-MEKK1 was localized in the cytoplasm, p-MEKK1 was localized in the nuclear membrane and cytoplasm, and p-ERK1/2 was localized in the cytoplasm and nucleus. ⑤ After API was applied to cells, the expressions of p-MEKK1 and p-ERK1/2 proteins significantly reduced (P<0.01).

Conclusion: Apigenin (API) significantly inhibits the proliferation, migration, and invasion of Tca8113 cells and its mechanism may be associated with the MAPK signaling pathway.

Keywords: Apigenin (API), Tca8113 cell, mitogen-activated protein kinase signaling pathways, cell proliferation, MTT, ERK.

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