微钙化（MC）是乳腺癌的一个有价值的诊断指标，据报道它与肿瘤侵袭性增加和预后不良有关。然而，确切的潜在分子机制尚未完全了解。在这里，我们发现矿化的浸润性乳腺癌（IBC）细胞不仅增加了增殖和迁移，而且还表现出阿霉素耐药的特征。 PI3K/AKT信号通路与IBC钙化的产生相关，并激活其下游缺氧诱导因子1α（HIF1α）的转录和翻译。 HIF1α 蛋白的敲低显着下调细胞增殖和迁移，同时钙化持续存在。与此同时，由于 HIF1α 表达受到抑制，钙化乳腺癌细胞恢复了对阿霉素的敏感性。此外，我们还提供了 HIF1α 作为阿霉素耐药性生物标志物的潜在价值的初始数据。这些发现为探索 IBC 中的微钙化提供了新方向。© 2023。作者。

Microcalcification (MC) is a valuable diagnostic indicator of breast cancer, and it is reported to be associated with increased tumor aggressiveness and poor prognosis. Nevertheless, the exact potential molecular mechanism is not completely understood. Here, we find that the mineralized invasive breast cancer (IBC) cells not only increased their proliferation and migration, but also showed the characteristic of doxorubicin resistance. The PI3K/AKT signaling pathway is associated with the generation of calcification in IBC, and it activates the transcription and translation of its downstream hypoxia-inducible factor 1α (HIF1α). Knockdown of HIF1α protein significantly downregulated cell proliferation and migration while calcification persists. Meanwhile, calcified breast cancer cells restored sensitivity to doxorubicin because of suppressed HIF1α expression. In addition, we provide initial data on the underlying value of HIF1α as a biomarker of doxorubicin resistance. These findings provide a new direction for exploring microcalcifications in IBC.© 2023. The Author(s).