乳腺癌患者往往预后不良，很大程度上是由于缺乏有效的靶向治疗。现已证实，单糖可增强肿瘤细胞的生长迟缓和化疗敏感性。然而，果胶糖是否具有限制肿瘤细胞增殖的能力尚不清楚。在此，我们报道乳腺癌细胞系中果胶糖诱导的细胞毒性是通过自噬和 p38 MAPK 信号通路调节的。果胶暴露以剂量依赖性方式显着抑制细胞增殖，这与细胞周期停滞相关，如 G2/M 细胞周期限制和 Cyclin A、Cyclin B、p21 和 p27 的异位表达所证明。从机制上讲，我们进一步发现果胶糖与乳腺癌中的自噬和 p38 MAPK 信号传导呈正相关。相比之下，自噬或 p38 MAPK 抑制剂 3-Ma 或 SB203580 逆转了果胶糖对乳腺癌细胞系增殖和细胞周期过程的抑制功效。此外，果胶糖体内治疗可以显着抑制乳腺癌细胞的异种移植生长。总而言之，我们的研究结果首次揭示了果胶糖通过激活乳腺癌细胞中的 p38 MAPK 信号通路诱导自噬，从而引发细胞周期停滞，尤其是在管腔 A 型乳腺癌和三阴性乳腺癌中。© 2024。 ）。

Breast cancer patients often have a poor prognosis largely due to lack of effective targeted therapy. It is now well established that monosaccharide enhances growth retardation and chemotherapy sensitivity in tumor cells. However, Pectinose whether has capability to restrict the proliferation of tumor cells remain unclear. Here, we report that Pectinose induced cytotoxicity is modulated by autophagy and p38 MAPK signaling pathway in breast cancer cell lines. The proliferation of cells was dramatically inhibited by Pectinose exposure in a dose-dependent manner, which was relevant to cell cycle arrest, as demonstrated by G2/M cell cycle restriction and ectopic expression of Cyclin A, Cyclin B, p21and p27. Mechanistically, we further identified that Pectinose is positively associated with autophagy and the activation of the p38 MAPK signaling in breast cancer. In contrast, 3-Ma or SB203580, the inhibitor of autophagy or p38 MAPK, reversed the efficacy of Pectinose suppressing on breast cancer cell lines proliferation and cell cycle process. Additionally, Pectinose in vivo treatment could significantly inhibit xenograft growth of breast cancer cells. Taken together, our findings were the first to reveal that Pectinose triggered cell cycle arrest by inducing autophagy through the activation of p38 MAPK signaling pathway in breast cancer cells,especially in luminal A and triple-negative breast cancer.© 2024. The Author(s).