Abstract：
Baicalin was reported to facilitate the apoptosis of colon cells and inhibit tumor growth in vivo. This study aimed to explore the specific mechanism and function of baicalin on colon cells. Relative mRNA levels were tested via qPCR. Cell proliferation, viability, and cell cycle phases were evaluated using MTT, colony formation, and flow cytometry assays, respectively. The interaction between miR-139-3p and cyclin-dependent kinase 16 (CDK16) was measured via a dual-luciferase reporter assay. Immunohistochemistry was used to count the positivity cells in tumor tissues collected from treated xenografted tumor mice. The results showed that baicalin increased miR-139-3p expression while also decreasing CDK16 levels, blocking the cell cycle, and inhibiting cell proliferation in colon cancer cells. miR-139-3p silencing or CDK16 overexpression abolished the inhibitory effects of baicalin on colon cancer proliferation. miR-139-3p directly targeted and interacted with CDK16 at the cellular level. The protective functions of miR-139-3p knockdown on tumor cells were abrogated by silencing CDK16. The combination of baicalin treatment and CDK16 knockdown further inhibited tumor growth of xenografted tumor mice compared with the groups injected with only sh-CDK16 or baicalin in vivo. In conclusion, baicalin inhibited colon cancer growth by modulating the miR-139-3p/CDK16 axis.
摘要：
据报道黄芩苷在体内促进结肠细胞凋亡并抑制肿瘤生长。本研究旨在探讨黄芩苷对结肠细胞的作用机制和功能。通过qPCR测试相对mRNA水平。细胞增殖，生存能力，使用MTT评估细胞周期阶段，菌落形成,和流式细胞术检测，分别。miR-139-3p与细胞周期蛋白依赖性激酶16(CDK16)之间的相互作用通过双荧光素酶报告基因测定来测量。使用免疫组织化学对从处理的异种移植肿瘤小鼠收集的肿瘤组织中的阳性细胞进行计数。结果表明，黄芩苷增加miR-139-3p表达，同时降低CDK16水平，阻断细胞周期,并抑制结肠癌细胞的细胞增殖。miR-139-3p沉默或CDK16过表达消除了黄芩苷对结肠癌增殖的抑制作用。miR-139-3p在细胞水平上直接靶向并与CDK16相互作用。miR-139-3p敲低对肿瘤细胞的保护功能通过沉默CDK16被废除。与体内仅注射sh-CDK16或黄芩苷的组相比,黄芩苷治疗和CDK16敲低的组合进一步抑制异种移植肿瘤小鼠的肿瘤生长。总之,黄芩苷通过调节miR-139-3p/CDK16轴抑制结肠癌生长。
