The molecular pathogenesis of colorectal cancer (CRC) has been widely investigated in recent years. Accumulating evidence has indicated that microRNA (miRNA) dysregulation participates in the processes of driving CRC initiation and progression. Aberrant expression of miR-1301 has been found in various tumor types. However, its role in CRC remains to be elucidated. In the present study, we identified miR-1301 was enriched in normal colorectal tissues and significantly down-regulated in CRC. Decreased level of miR-1301 strongly correlated with aggressive pathological characteristics, including advanced stage and metastasis. Bioinformatics and dual luciferase assay demonstrated that STAT3 is a direct target of miR-1301. Gain and loss-of-function assays showed that miR-1301 had no effect on cell proliferation. Overexpression of miR-1301 suppressed cell migration and invasion capacity of pSTAT3-positive LoVo cells, but not pSTAT3-negative SW480 cells, while inhibition of miR-1301 consistently promoted cell migration and invasion in both cell lines. Additionally, miR-1301 inhibition restored the suppressed migration and invasion of STAT3-knockdown LoVo cells. MiR-1301 functioned as a tumor suppressor to modulate the IL6/STAT3 signaling pathway. In summary, this study highlights the significant role of miR-1301/STAT3 axis in CRC metastasis.

中文翻译：

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miR-1301水平降低通过激活STAT3通路促进结直肠癌进展

近年来，结直肠癌（CRC）的分子发病机制得到了广泛研究。越来越多的证据表明，microRNA (miRNA) 失调参与了驱动 CRC 发生和进展的过程。已在各种肿瘤类型中发现 miR-1301 的异常表达。然而，其在 CRC 中的作用仍有待阐明。在本研究中，我们发现 miR-1301 在正常结直肠组织中富集，在 CRC 中显着下调。miR-1301 水平降低与侵袭性病理特征密切相关，包括晚期和转移。生物信息学和双荧光素酶测定表明 STAT3 是 miR-1301 的直接靶标。功能获得和功能丧失检测表明 miR-1301 对细胞增殖没有影响。miR-1301 的过表达抑制 pSTAT3 阳性 LoVo 细胞的细胞迁移和侵袭能力，但不抑制 pSTAT3 阴性 SW480 细胞，而抑制 miR-1301 始终促进两种细胞系中的细胞迁移和侵袭。此外，抑制 miR-1301 恢复了抑制 STAT3 敲低的 LoVo 细胞的迁移和侵袭。MiR-1301 作为肿瘤抑制因子调节 IL6/STAT3 信号通路。总之，本研究强调了 miR-1301/STAT3 轴在 CRC 转移中的重要作用。MiR-1301 作为肿瘤抑制因子调节 IL6/STAT3 信号通路。总之，本研究强调了 miR-1301/STAT3 轴在 CRC 转移中的重要作用。MiR-1301 作为肿瘤抑制因子调节 IL6/STAT3 信号通路。总之，本研究强调了 miR-1301/STAT3 轴在 CRC 转移中的重要作用。