As a flavonoid, baicalein exhibits remarkable anti-cancer roles in several cancers. However, the factors regulating the antitumorigenic roles of baicalein in cervical cancer remain undefined. Here, we revealed that long noncoding RNA SNHG1 is implicated in the tumor-suppressive roles of baicalein. Functional assays demonstrated that ectopic expression of SNHG1 attenuates the roles of baicalein in repressing cervical cancer cell viability, inducing apoptosis, and repressing migration. SNHG1 silencing promotes the tumor-suppressive roles of baicalein in cervical cancer cell viability, apoptosis, and migration. Xenograft assays showed that SNHG1 reverses the tumor-suppressive roles of baicalein in repressing cervical cancer growth in vivo. Mechanistic investigations revealed that SNHG1 directly binds miR-3127-5p and up-regulates FZD4, a target of miR-3127-5p. Via regulating miR-3127-5p/FZD4, SNHG1 activates Wnt/β-catenin signaling. Moreover, SNHG1 reverses the repressive role of baicalein on Wnt/β-catenin signaling. The effect of SNHG1 on the antitumorigenic process of baicalein was abolished by Wnt/β-catenin signaling inhibitor ICG-001. Together, our observations demonstrated that SNHG1 represses the tumor-suppressive roles of baicalein in cervical cancer through regulating miR-3127-5p/FZD4/Wnt/β-catenin axis, and suggested that targeting SNHG1 represents a potential strategy to enhance the tumor-suppressive roles of baicalein in cervical cancer.

Impact statement

Baicalein exhibits anti-cancer roles in several cancers. However, the factors influencing the antitumorigenic efficiencies of baicalein in CC remain largely unclear. Here, we provide convincing evidences that lncRNA SNHG1 attenuates the tumor-suppressive roles of baicalein in CC cell viability, apoptosis, migration, and CC tumor growth. This study further demonstrates that the influences of SNHG1 in the antitumorigenic process of baicalein are achieved through modulating the miR-3127-5p/FZD4Wnt/β-catenin axis. SNHG1 attenuates the repressive role of baicalein on Wnt/β-catenin. Therefore, SNHG1 is a novel modulator of the tumor-suppressive roles of baicalein and SNHG1 represents a therapeutic intervention target to reinforce the tumor-suppressive roles of baicalein in CC.

中文翻译：

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SNHG1 通过调节 miR-3127-5p/FZD4/Wnt/β-catenin 信号传导抑制黄芩素在宫颈癌中的抗癌作用。

作为一种类黄酮，黄芩素在多种癌症中表现出显着的抗癌作用。然而，调节黄芩素在宫颈癌中的抗肿瘤作用的因素仍不清楚。在这里，我们发现长非编码 RNA SNHG1 与黄芩素的肿瘤抑制作用有关。功能分析表明，SNHG1 的异位表达减弱了黄芩素在抑制宫颈癌细胞活力、诱导细胞凋亡和抑制迁移方面的作用。 SNHG1 沉默促进黄芩素在宫颈癌细胞活力、细胞凋亡和迁移中的肿瘤抑制作用。异种移植试验表明，SNHG1 可以逆转黄芩素在体内抑制宫颈癌生长的肿瘤抑制作用。机制研究表明，SNHG1 直接结合 miR-3127-5p 并上调 FZD4（miR-3127-5p 的靶标）。通过调节 miR-3127-5p/FZD4，SNHG1 激活 Wnt/β-catenin 信号传导。此外，SNHG1 逆转黄芩素对 Wnt/β-连环蛋白信号传导的抑制作用。 Wnt/β-catenin 信号抑制剂 ICG-001 消除了 SNHG1 对黄芩素抗肿瘤过程的影响。总之，我们的观察结果表明，SNHG1 通过调节 miR-3127-5p/FZD4/Wnt/β-catenin 轴来抑制黄芩素在宫颈癌中的肿瘤抑制作用，并表明靶向 SNHG1 是增强肿瘤抑制作用的潜在策略。黄芩素在宫颈癌中的作用。

 影响报告

黄芩素在多种癌症中表现出抗癌作用。然而，影响黄芩素在 CC 中抗肿瘤作用的因素仍不清楚。在这里，我们提供了令人信服的证据，表明 lncRNA SNHG1 减弱了黄芩素在 CC 细胞活力、细胞凋亡、迁移和 CC 肿瘤生长中的肿瘤抑制作用。本研究进一步证明SNHG1在黄芩素抗肿瘤过程中的影响是通过调节miR-3127-5p/FZD4Wnt/β-catenin轴来实现的。 SNHG1 减弱黄芩素对 Wnt/β-连环蛋白的抑制作用。因此，SNHG1 是黄芩素的肿瘤抑制作用的新型调节剂，并且 SNHG1 代表了增强黄芩素在 CC 中的肿瘤抑制作用的治疗干预靶点。