Hebp2, also known as heme-binding protein 2, has been implicated in multiple biological processes. It may be involved in facilitating necrotic cell death under oxidative stress. Additionally, the interaction between apoptosis-linked gene 2 (ALG-2) and Hebp2 seems to play a role in regulating microtubule cytoskeleton, which impacts mitotic spindle function. This connection is significant as genomic instability in cancer cells can arise from improper microtubule regulation [2].

In triple-negative breast cancer (TNBC), overexpression of Hebp2 enhanced the viability of MDA-MB-231 cells in response to cisplatin and BCNU, while Nuclease technology-mediated Hebp2-knockout reduced cell viability in response to these drugs. This indicates that Hebp2 may play a role in resistance to cisplatin and BCNU, which induce DNA cross-links, in TNBC cells [1].

In ovarian cancer, Hebp2, a fatty acid-associated gene, not only accelerates cancer progression but also drives the polarization from M0_TAM to M2_TAM, modifying the immune landscape and leading to carboplatin resistance. Both in vitro and in vivo experiments showed its role in promoting the proliferation of resistant cell lines and suppressing apoptosis [3].

In conclusion, Hebp2 has functions related to cell death, microtubule regulation, and is involved in cancer drug resistance in breast and ovarian cancers. Studies using gene-editing techniques like Nuclease technology in cell models have been crucial in revealing these functions, providing potential targets for cancer treatment strategies.