Department of Gynecology and Obstetrics, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China (mainland).
Department of Obstetrics and Gynecology, The Second People's Hospital of Lianyungang City, Lianyungang, Jiangsu, China (mainland).
Med Sci Monit. 2020 Oct 20;26:e926780. doi: 10.12659/MSM.926780.
BACKGROUND Cervical cancer threatens women's health worldwide. Verteporfin (VP), a small-molecule YAP1 inhibitor, inhibits cancer cell growth. This study investigated whether VP could inhibit the proliferation and promote the apoptosis of cervical cancer cells by decreasing SULT2B1 expression. MATERIAL AND METHODS Normal and cancerous cervical cell proliferation after VP treatment was detected by CCK-8 assay. HeLa cell migration, invasion, and apoptosis after VP treatment and transfection were analyzed by wound healing assay, transwell assay, and TUNEL assay, respectively. The expression of related proteins was determined by western blot analysis. Western blot and RT-qPCR analysis detected mRNA and protein expression of SULT2B1. RESULTS Different VP concentrations (0.5, 1, 2, and 5 μM) inhibited the viability of HeLa cells and had no obvious effect on H8 cells. Therefore, 5 μM VP was selected for subsequent experiments. VP inhibited the proliferation, migration, and invasion of HeLa cells and promoted their apoptosis. Bcl-2 expression decreased, and expression of Bax, caspase-3, and caspase-9 in VP-treated HeLa cells increased. SULT2B1 expression increased in cervical cancer cells compared with normal cervical cells. Furthermore, SULT2B1 expression increased in HeLa cells and VP suppressed SULT2B1 expression. SULT2B1 overexpression reduced the inhibiting effect of VP on the proliferation, migration, and apoptosis of HeLa cells, and reduced VP effect on apoptosis of HeLa cells. SULT2B1 overexpression upregulated the Bcl-2 expression and downregulated the expression of Bax, caspase-3, and caspase-9 in VP-treated HeLa cells. CONCLUSIONS VP inhibited the proliferation, migration, and invasion and promoted apoptosis of cervical cancer cells by decreasing SULT2B1 expression.
宫颈癌威胁着全世界女性的健康。维替泊芬（VP）是一种小分子 YAP1 抑制剂，可抑制癌细胞生长。本研究旨在探讨维替泊芬能否通过降低 SULT2B1 表达来抑制宫颈癌细胞增殖并促进其凋亡。
通过 CCK-8 法检测 VP 处理后正常和癌变宫颈细胞的增殖情况。通过划痕愈合实验、Transwell 实验和 TUNEL 实验分别分析 VP 处理和转染后 HeLa 细胞的迁移、侵袭和凋亡情况。通过 Western blot 分析检测相关蛋白的表达。Western blot 和 RT-qPCR 分析检测 SULT2B1 的 mRNA 和蛋白表达。
不同浓度的 VP（0.5、1、2 和 5 μM）抑制了 HeLa 细胞的活力，但对 H8 细胞没有明显影响。因此，选择 5 μM VP 进行后续实验。VP 抑制了 HeLa 细胞的增殖、迁移和侵袭，并促进了其凋亡。Bcl-2 表达减少，VP 处理的 HeLa 细胞中 Bax、caspase-3 和 caspase-9 的表达增加。与正常宫颈细胞相比，宫颈癌细胞中 SULT2B1 的表达增加。此外，SULT2B1 在 HeLa 细胞中的表达增加，而 VP 抑制了 SULT2B1 的表达。SULT2B1 过表达降低了 VP 对 HeLa 细胞增殖、迁移和凋亡的抑制作用，并降低了 VP 对 HeLa 细胞凋亡的作用。SULT2B1 过表达上调了 VP 处理的 HeLa 细胞中 Bcl-2 的表达，下调了 Bax、caspase-3 和 caspase-9 的表达。
VP 通过降低 SULT2B1 表达抑制宫颈癌细胞的增殖、迁移和侵袭，促进其凋亡。
