Oncogenic viral infection triggers LAMP2A SUMOylation and chaperone-mediated autophagy to promote tumorigenesis.

Oncogenic viruses induce LAMP2A SUMOylation via TRIM32, activating CMA to promote tumor growth and viral persistence in vivo.

• Why it matters: Understanding how viruses manipulate autophagy pathways is crucial for developing targeted therapies against virus-associated cancers, which often resist current treatments.
• What they did: The study used Kaposi's sarcoma-associated herpesvirus as a model to show that TRIM32 mediates SUMO2/3 conjugation to LAMP2A at specific lysine residues, leading to CMA activation.
• The result: Inhibitors targeting SUMOylated LAMP2A exhibit strong antitumor and antiviral effects in vitro and in mice, highlighting LAMP2A as a promising therapeutic target for virus-related cancers.