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The Anti-tumor Effects of p-Coumaric Acid on Melanoma A375 and B16 Cells

Hu, Xue, Yang, Zihui, Liu, Wenjing, Pan, Zhaohai, Zhang, Xin, Li, Minjing, Liu, Xiaona, Zheng, Qiusheng, Li, Defang·2020·Frontiers in Oncology
DOI 10.3389/fonc.2020.558414PMC PMC7597589
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Figure 1 p-CA inhibits proliferation and colony formation of A375 and B16 cells. (A,B) A375 and B16 cells were treated with p-CA. After incubation for 24 or 48 h, the proliferation rates of A375 and B16 cells were measured by CCK-8 assay. (C) HaCaT, A375 and B16 cells were treated with p-CA. After incubation for 24 h, the proliferation rates of HaCaT, A375 and B16 cells were measured by CCK-8 assay. (D) Morphological changes of p-CA-treated HaCaT cells were observed under a phase contrast microscope. (E) Morphological changes of A375 and B16 cells were observed under a phase contrast microscope. Scale bar, 50 μm. (F) The cell colonies were stained with crystal violet and observed under an inverted microscope. All data are expressed as the mean ± SD of three independent experiments. &P < 0.05 compared with the A375 or B16 cells after p-CA treatment for 24 h. *P < 0.05, **P < 0.01, #P < 0.05, ##P < 0.01 compared with the control.
Figure 1 p-CA inhibits proliferation and colony formation of A375 and B16 cells. (A,B) A375 and B16 cells were treated with p-CA. After incubation for 24 or 48 h, the proliferation rates of A375 and B16 cells were measured by CCK-8 assay. (C) HaCaT, A375 and B16 cells were treated with p-CA. After incubation for 24 h, the proliferation rates of HaCaT, A375 and B16 cells were measured by CCK-8 assay. (D) Morphological changes of p-CA-treated HaCaT cells were observed under a phase contrast microscope. (E) Morphological changes of A375 and B16 cells were observed under a phase contrast microscope. Scale bar, 50 μm. (F) The cell colonies were stained with crystal violet and observed under an inverted microscope. All data are expressed as the mean ± SD of three independent experiments. &P < 0.05 compared with the A375 or B16 cells after p-CA treatment for 24 h. *P < 0.05, **P < 0.01, #P < 0.05, ##P < 0.01 compared with the control.CC BY · PubMed Central
Figure 2 p-CA causes A375 and B16 cell cycle arrest. (A) The cell cycle distribution of A375 cells treated with p-CA was measured by flow cytometry. (B) Statistical analysis of the cell cycle distribution of A375 cells treated with p-CA. (C) The cell cycle distribution of B16 cells treated with p-CA was measured by flow cytometry. (D) Statistical analysis of the cell cycle distribution of B16 cells treated with p-CA. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the control.
Figure 2 p-CA causes A375 and B16 cell cycle arrest. (A) The cell cycle distribution of A375 cells treated with p-CA was measured by flow cytometry. (B) Statistical analysis of the cell cycle distribution of A375 cells treated with p-CA. (C) The cell cycle distribution of B16 cells treated with p-CA was measured by flow cytometry. (D) Statistical analysis of the cell cycle distribution of B16 cells treated with p-CA. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the control.CC BY · PubMed Central
Figure 3 p-CA regulates the activity of Cyclin–CDK complexes and cell cycle progression. (A) The protein levels of Cyclin A and CDK2 in A375 cells treated with p-CA, as measured by western blot. (B) Statistical analysis of Cyclin A and CDK2 levels in A375 cells. The ratio of protein levels was standardized according to the value of the control. (C) The protein levels of Cyclin E and CDK2 in B16 cells treated with p-CA, as measured by western blot. (D) Statistical analysis of Cyclin E and CDK2 levels in B16 cells. The ratio of protein levels was standardized according to the value of the control. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the control.
Figure 3 p-CA regulates the activity of Cyclin–CDK complexes and cell cycle progression. (A) The protein levels of Cyclin A and CDK2 in A375 cells treated with p-CA, as measured by western blot. (B) Statistical analysis of Cyclin A and CDK2 levels in A375 cells. The ratio of protein levels was standardized according to the value of the control. (C) The protein levels of Cyclin E and CDK2 in B16 cells treated with p-CA, as measured by western blot. (D) Statistical analysis of Cyclin E and CDK2 levels in B16 cells. The ratio of protein levels was standardized according to the value of the control. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the control.CC BY · PubMed Central
Figure 4 p-CA induces A375 and B16 cell apoptosis. (A,B) After Hoechst 33,258 staining, the nucleus of A375 and B16 cells treated with p-CA showed morphological changes typical of apoptosis. (C) The apoptosis rate of A375 cells treated with p-CA was measured by Annexin V-FITC/PI double staining. (D) Statistical analysis of the apoptosis rate of A375 cells treated with p-CA. (E) The apoptosis rate of B16 cells treated with p-CA was measured by Annexin V-FITC/PI double staining. (F) Statistical analysis of the apoptosis rate of B16 cells treated with p-CA. All data are expressed as the mean ± SD of three independent experiments. **P < 0.01 compared with the control.
Figure 4 p-CA induces A375 and B16 cell apoptosis. (A,B) After Hoechst 33,258 staining, the nucleus of A375 and B16 cells treated with p-CA showed morphological changes typical of apoptosis. (C) The apoptosis rate of A375 cells treated with p-CA was measured by Annexin V-FITC/PI double staining. (D) Statistical analysis of the apoptosis rate of A375 cells treated with p-CA. (E) The apoptosis rate of B16 cells treated with p-CA was measured by Annexin V-FITC/PI double staining. (F) Statistical analysis of the apoptosis rate of B16 cells treated with p-CA. All data are expressed as the mean ± SD of three independent experiments. **P < 0.01 compared with the control.CC BY · PubMed Central
Figure 5 Effects of p-CA on apoptosis-related proteins. (A) The protein levels of caspase-3/9 and cleaved caspase-3/9 in A375 cells treated with p-CA were measured by western blot. (B) The relative protein levels of caspase-3/9 and cleaved caspase-3/9 in A375 cells treated with p-CA were statistically analyzed. (C) The protein levels of caspase-3/9 and cleaved caspase-3/9 in B16 cells treated with p-CA were measured by western blot. (D) The relative protein levels of caspase-3/9 and cleaved caspase-3/9 in B16 cells treated with p-CA were statistically analyzed. The ratio of protein levels is normalized according to the value of the control group. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the control.
Figure 5 Effects of p-CA on apoptosis-related proteins. (A) The protein levels of caspase-3/9 and cleaved caspase-3/9 in A375 cells treated with p-CA were measured by western blot. (B) The relative protein levels of caspase-3/9 and cleaved caspase-3/9 in A375 cells treated with p-CA were statistically analyzed. (C) The protein levels of caspase-3/9 and cleaved caspase-3/9 in B16 cells treated with p-CA were measured by western blot. (D) The relative protein levels of caspase-3/9 and cleaved caspase-3/9 in B16 cells treated with p-CA were statistically analyzed. The ratio of protein levels is normalized according to the value of the control group. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the control.CC BY · PubMed Central
Figure 6 p-CA induces A375 and B16 cell apoptosis through the Bcl-2/Bax signaling pathway. (A) The protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in A375 cells treated with p-CA were measured by western blot. (B) Statistical analysis of the relative protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in A375 cells treated with p-CA. The ratio of protein levels was normalized according to the value of the control. (C) The protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in B16 cells treated with p-CA were measured by western blot. (D) Statistical analysis of the relative protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in B16 cells treated with p-CA. The ratio of protein levels was normalized according to the value of the control. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the corresponding control.
Figure 6 p-CA induces A375 and B16 cell apoptosis through the Bcl-2/Bax signaling pathway. (A) The protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in A375 cells treated with p-CA were measured by western blot. (B) Statistical analysis of the relative protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in A375 cells treated with p-CA. The ratio of protein levels was normalized according to the value of the control. (C) The protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in B16 cells treated with p-CA were measured by western blot. (D) Statistical analysis of the relative protein levels of Apaf1, cytoplasmic Cyto-C, Bax, and Bcl-2 in B16 cells treated with p-CA. The ratio of protein levels was normalized according to the value of the control. All data are expressed as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 compared with the corresponding control.CC BY · PubMed Central

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Metadata

Authors
Hu, X., Yang, Z., Liu, W., Pan, Z., Zhang, X., Li, M., Liu, X., Zheng, Q., & Li, D.
Venue
Frontiers in Oncology
Publisher
Frontiers Media SA
Published
2020-10-16
Volume
10
ISSN
2234-943X
DOI
10.3389/fonc.2020.558414
PMC
PMC7597589
Cited by
65
References
0
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Innovative Research Group Project of the National Natural Science Foundation of China (31870338, 81872162)

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Hu, X., Yang, Z., Liu, W., Pan, Z., Zhang, X., Li, M., Liu, X., Zheng, Q., & Li, D. (2020). The Anti-tumor Effects of p-Coumaric Acid on Melanoma A375 and B16 Cells. Frontiers in Oncology. https://doi.org/10.3389/fonc.2020.558414

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