Data Sheet 1_Caprine herpes virus-1 reduces cell viability and enhances chemosensitivity in breast cancer cells.zip

IntroductionOncolytic viruses (OVs) are promising therapeutic agents in oncology that directly lyse tumor cells, modulate the immune response, and alter the tumor microenvironment. Non-human OVs offer advantages over their human counterparts, such as being non-pathogenic in humans and lacking pre-existing immunity. In previous studies, we demonstrated that a non-human caprine herpesvirus 1 (CpHV-1) effectively kills various human cancer cell lines. In this study, we evaluate CpHV-1’s antitumor effects across different breast cancer (BC) cell lines and its potential synergy with FDA-approved BC therapies.
MethodsWe assessed the effects of CpHV-1 on BC cell viability and clonogenic potential, cell cycle regulation, and apoptosis in MCF-7, T47D, SKBR3, and MDA-MB-468 cell lines, as well as in non-tumorigenic mammary epithelial cells (MCF-10A). Additionally, CpHV-1 was tested in combination with Abemaciclib, Tucatinib, and Inavolisib, and synergism was evaluated using Chou–Talalay analysis.
ResultsOur data show that CpHV-1 induced a dose-dependent cytotoxic effect, with an MOI of 5 reducing viability by ~50% 72 hours post-infection. Clonogenic assays confirmed long-term growth inhibition. We also demonstrated modulation of cell cycle progression and induction of apoptosis in tumor cells mediated by CpHV-1. Finally, combined treatments showed synergy across all BC subtypes, without significant toxicity in normal cells.
DiscussionThese findings highlight CpHV-1 as a promising oncolytic agent capable of targeting multiple breast cancer subtypes. Its ability to significantly reduce viability, impair long-term proliferation, and induce apoptosis, together with its synergistic activity when combined with FDA-approved targeted therapies and its limited toxicity in normal cells, supports further investigation of CpHV-1 for breast cancer treatment.