ALDH1A3 and Linc00284 involve in colorectal cancer (CRC) development; however, the regulatory mechanism is still unclear. In this study, we collected clinicopathological characteristics and tissue samples from 73 CRC patients to analyze the expression of ALDH1A3, Linc00284, TGFβ signaling and miR-361-5p using qPCR, Western blotting, and ELISA. Multiple CRC cell lines were evaluated in this study, and the highest level of ALDH1A3 was observed in SW480 cells. To investigate the regulatory mechanism, RIP and luciferase assays were used to validate the interaction between Linc00284, miR-361-5p, and TGFβ. Proliferation, viability, migration, and invasion assays were performed to profile the effects of the ALDH1A3–Linc00284 axis in CRC cell functions, which was upregulated in CRC tissues. Knockdown ALDH1A3 or Linc00284 significantly reduced TGFβ expression and suppressed the EMT process, while overexpression had opposite effects. miR-361-5p targeted TGFβ directly, which negatively correlated with ALDH1A3–Linc00284 expression and CRC progression. Mechanistically, upregulation of ALDH1A3–Linc00284 promotes colorectal cancer invasion and migration by regulating miR-361-5p/TGFβ signaling pathway. Dysregulation of the ALDH1A3–Linc00284-miR-361-5p-TGFβ axis causes CRC invasion, which might provide a new insight into the treatment of CRC.

中文翻译：

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ALDH1A3–Linc00284 Axis 通过海绵 miR-361-5p 靶向 TGFβ 信号传导介导结肠直肠癌的侵袭

ALDH1A3 和 Linc00284 参与结直肠癌 (CRC) 的发展；然而，监管机制仍不清楚。在这项研究中，我们收集了 73 名 CRC 患者的临床病理特征和组织样本，使用 qPCR、Western blotting 和 ELISA分析了 ALDH1A3、Linc00284、TGF β信号和 miR-361-5p 的表达。本研究评估了多个 CRC 细胞系，在 SW480 细胞中观察到最高水平的 ALDH1A3。为了研究调控机制，使用 RIP 和荧光素酶测定来验证 Linc00284、miR-361-5p 和 TGF β之间的相互作用. 进行增殖、活力、迁移和侵袭测定以分析 ALDH1A3-Linc00284 轴在 CRC 细胞功能中的影响，该轴在 CRC 组织中上调。敲低 ALDH1A3 或 Linc00284 显着降低 TGF β表达并抑制 EMT 过程，而过表达则具有相反的效果。miR-361-5p 直接靶向 TGF β，这与 ALDH1A3-Linc00284 表达和 CRC 进展呈负相关。机制上，ALDH1A3-Linc00284 的上调通过调节 miR-361-5p/TGF β信号通路促进结直肠癌的侵袭和迁移。ALDH1A3-Linc00284-miR-361-5p-TGFβ轴的失调导致CRC侵袭，这可能为CRC的治疗提供新的见解。