Poriaic Acid Affecting Epithelial-Mesenchymal Transition and Apoptosis of A549/DDP Cells via Glycogen Synthesis Kinase-3β/Snail Signaling Pathway

Background: The paper explored the mechanism of Poriaic acid-containing serum interfering with EMT and apoptosis of A549/DDP cells. The aim is to find experimental evidence of Poriaic acid intervening cisplatin resistance in lung cancer, searching for effective targets, and to explore the mechanism of cisplatin resistance in lung cancer. Material and methods: Immunochemistry and western blotting were employed to detect the effects of Poriaic acid-containing serum on the expressions of p-GSK-3β (ser9), Snail protein and mRNA in GSK-3β/Snail signaling pathway, and the effects of Poriaic acid-containing serum on the expressions of EMT markers and related apop-totic factors. Results: The results of immunoblotting and immunocytochemistry rendered that the expressions of p-GSK-3β (ser9), Snail protein and mRNA decreased in the administration group as contrast to the blank group. As to the effect of Poriaic acid-containing serum on EMT markers, the immunoblotting results showed that the E-cadherin protein and mRNA expressions increased while the expressions of N-cadherin protein and mRNA decreased. Poriaic acid-containing serum can up-regulate the expressions of P53, Bax protein and mRNA, and down-regulate the expressions of Bcl-2 protein and mRNA. Conclusion: Poriaic acid-containing serum can affect EMT and apoptosis of A549/DDP cells by interfering with GSK-3β/Snail signaling pathway.

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ARHGAP10 inhibits the epithelial–mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway

Cancer Cell International ◽

10.1186/s12935-021-02022-7 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Lan-Lan Lin ◽

Fan Yang ◽

Dong-Huan Zhang ◽

Cong Hu ◽

Sheng Yang ◽

...

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Signaling Pathway ◽

Cell Lung Cancer ◽

Rho Gtpase ◽

Epithelial Mesenchymal Transition ◽

Essential Element ◽

Small Cell ◽

Small Cell Lung ◽

Mesenchymal Transition

Abstract Background Rho GTPase activating protein 10 (ARHGAP10) has been implicated as an essential element in multiple cellular process, including cell migration, adhesion and actin cytoskeleton dynamic reorganization. However, the correlation of ARHGAP10 expression with epithelial–mesenchymal transition (EMT) in lung cancer cells is unclear and remains to be elucidated. Herein, we investigated the relationship between the trait of ARHGAP10 and non-small cell lung cancer (NSCLC) pathological process. Methods Immunohistochemistry was conducted to evaluate the expression of ARHGAP10 in NSCLC tissues. CCK-8 assays, Transwell assays, scratch assays were applied to assess cell proliferation, invasion and migration. The expression levels of EMT biomarkers and active molecules involved in PI3K/Akt/GSK3β signaling pathway were examined through immunofluorescence and Western blot. Results ARHGAP10 was detected to be lower expression in NSCLC tissues compared with normal tissues from individuals. Moreover, overexpression of ARHGAP10 inhibited migratory and invasive potentials of A549 and NCI-H1299 cells. In addition, ARHGAP10 directly mediated the process of EMT via PI3K/Akt/GSK3β pathway. Meanwhile, activation of the signaling pathway of insulin-like growth factors-1 (IGF-1) reversed ARHGAP10 overexpression regulated EMT in NSCLC cells. Conclusion ARHGAP10 inhibits the epithelial–mesenchymal transition in NSCLC via PI3K/Akt/GSK3β signaling pathway, suggesting agonist of ARHGAP10 may be an optional remedy for NSCLC patients than traditional opioids.

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