In 2015, T-VEC, an oncolytic virus derived from HSV-1, was the first of its kind approved for cancer treatment, particularly for melanoma, but its effectiveness is limited and mechanisms of HSV-1 replication in cancer cells are not well understood.
Researchers studied how BACH1, an interferon-stimulated gene, controls HSV-1 replication and discovered that its deficiency enhances the virus's ability to induce cancer cell death.
The findings suggest that targeting BACH1 could improve the effectiveness of HSV-1 in cancer therapies, evidenced by using hemin to boost antitumor activity and T cell infiltration in tumors.
The study investigates the role of the transcription factor SIX1 in the tumor microenvironment (TME) and its effect on tumor growth and immune cell infiltration.
Researchers found that higher levels of SIX1 in tumor tissues were linked to lower immune cell presence and worse survival rates for cancer patients.
Deleting SIX1 in cancer cells decreased tumor growth by boosting immune responses, highlighting its potential as a target for cancer immunotherapy through its influence on collagen production and immune activation.