Colorectal cancer (CRC) refers to a deadly carcinoma following potent invasiveness and metastasis in advanced stage. Unfortunately, existing anti‐CRC medicine is insufficient for chemotherapy in addition to adverse effects. Consequently, the candidate natural ingredient for treating CRC needs to be further developed. Our previous experiments report that genistein exerts beneficial effects to inhibit CRC cells via an antiproliferative mechanism. Based on the metastatic characteristics of staging CRC, anti‐invasive and antimetastatic pharmacological activities using genistein remain uninvestigated. The scientific purpose of this study was to disclose the antimetastatic mechanism by using human and cell culture/nude mice samples, followed by biochemical tests and immunoassays. In human study, these CRC cases resulted in increased transforming growth factor beta‐1 (TGF‐β1) levels, long noncoding RNA (lncRNA) TTTY18 expressions, followed with up‐regulated Ki‐67, serum and glucocorticoid regulated kinase 1 (SGK1), Akt^Ser473 expressions. In a study in vitro, genistein‐dosed CRC cells showed suppressed cell viability, promoted cell apoptosis, reduced Ki‐67 positive cells, reduced cellular migration, down‐regulated expressions of TTTY18, SGK1, Akt^Ser473, p38 MAPK^Tyr323. In a further study in vivo, genistein‐dosed tumor‐bearing nude mice exhibited visibly reduced body mass, lowered tumorous TGF‐β1 and TTTY18 contents. In addition, intracellular numbers of SGK1, Akt^Ser473, p38 MAPK^Tyr323 positive cells were reduced dose‐dependently. Collectively, these human and experimentative findings reveal that genistein pharmacologically exerts the potential antimetastatic CRC effects, possibly through a molecular mechanism of inhibiting TTTY18/Akt pathway in CRC cells.

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金雀异黄素对结直肠癌的抗侵袭作用及药理机制[J].

结直肠癌（CRC）是指在晚期发生有效侵袭和转移后的致命癌症。不幸的是，除了副作用外，现有的抗 CRC 药物不足以用于化疗。因此，需要进一步开发用于治疗结直肠癌的候选天然成分。我们之前的实验报告称，染料木黄酮通过抗增殖机制发挥抑制 CRC 细胞的有益作用。基于分期 CRC 的转移特征，使用染料木黄酮的抗侵袭和抗转移药理活性仍有待研究。本研究的科学目的是通过使用人类和细胞培养/裸鼠样本，然后进行生化测试和免疫分析来揭示抗转移机制。在人体研究中，^Ser473表达式。在一项体外研究中，注射染料木黄酮的 CRC 细胞显示出抑制细胞活力、促进细胞凋亡、减少 Ki-67 阳性细胞、减少细胞迁移、下调 TTTY18、SGK1、Akt ^Ser473、p38 MAPK ^{Tyr323 的表达}。在进一步的体内研究中，注射染料木黄酮的荷瘤裸鼠表现出明显的体重减轻、肿瘤性 TGF-β1 和 TTTY18 含量降低。此外，SGK1、Akt ^Ser473、p38 MAPK ^{Tyr323 的}胞内数阳性细胞呈剂量依赖性减少。总的来说，这些人类和实验发现表明，染料木黄酮在药理学上发挥了潜在的抗转移性 CRC 作用，可能是通过抑制 CRC 细胞中 TTTY18/Akt 通路的分子机制。