Abstract
Purpose Cinnamaldehyde (CA) is the main ingredient in cinnamon, and it has been proven to have an inhibitory effect on many different tumor types. However, it lacks effect on glioma. This paper explores the effect CA has on glioma cells U87 and U251 at the cellular and molecular levels. Methods The relationship between Hif-1α and Sept9 was found by CGGA. Cell Viability Assay (CCK8) was made to detect the proliferation ability. The scratch experiment and the transwell experiment were applied to the migration and invasion ability. Annexin V-FITC/PI were used to detect the cell apoptosis. Western blotting was used to determine the specified protein level. Results Cell proliferation assay results revealed CA to inhibit the proliferation of glioma cells in a dose-dependent manner. It promoted apoptosis for upregulating the expression of Bax and downregulating the expression of Bcl-2. Wound Healing Assay and transwell test found CA to have anti-invasion ability and that it upregulated the expression of E-cadherin and downregulated the expressions of MMP-2 and MMP-9. The molecular mechanism was studied from a tumor microenvironment (TME) perspective. Pi3k inhibitor (LY294002) was used for interfering with cells, and the results found CA to demonstrate a similar effect. Hif-1α and Sept9 expressions were inhibited, and Akt and p-Akt were also inhibited. By using CoCl2 to make hypoxia, CA was discovered to inhibit the high expression of Hif-1α and Sept9, demonstrating a correlation with the Pi3k/Akt pathway. It is suggested that the mechanism of Sept9 under hypoxia regulation can be realized through the Pi3k/Akt pathway. Conclusions This study proves for the first time that CA is an effective drug for inhibiting the proliferation of glioma through Sept9 and reveals Sept9 to be related to the Pi3k/Akt pathway in terms of tumor microenvironment, providing a molecular basis for the further study of CA in glioma treatment.
Highlights
Glioma is the most common tumor that is found in the brain’s nervous system
Experiments were conducted on this basis in order to confirm that CA can inhibit the expression of Sept9 and Hif-1α through the Pi3k/Akt pathway, inhibit the tumor microenvironment, and restrict tumor growth
LC3B was purchased from Bioss (Beijing China), Bcl-2 was purchased from Cell Signal Technology (Massachusetts, USA), rabbit anti-human antibody against Pi3k inhibitor LY 294002 was purchased from Cell Signal Technology (Massachusetts, USA), CoCl2 was purchased from Aladdin (Shanghai, China), CCK8 kit was purchased from Biosharp Life Sciences (Beijing, China), and Annexin V conjugated to fluorescein-isothiocyanate (Annexin V-FITC) apoptosis detection kit was purchased from Beyotime (Beijing, China)
Summary
Glioma is the most common tumor that is found in the brain’s nervous system Treatments for it include chemotherapy, radiotherapy, surgery, targeted therapy, and stem cell therapy. It can relapse, it has a high mortality rate, and the prognosis is poor [1]. It has been proven that cinnamaldehyde can inhibit the growth and invasiveness of cancer cells through the Pi3k/ Akt pathway. Experiments were conducted on this basis in order to confirm that CA can inhibit the expression of Sept and Hif-1α through the Pi3k/Akt pathway, inhibit the tumor microenvironment, and restrict tumor growth
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