Publications by authors named "Aobo He"
Chronic viral mimicry induction following p53 loss promotes immune evasion.
Cancer Discov
January 2025
Epigenetic therapies facilitate transcription of immunogenic repetitive elements that cull cancer cells through 'viral mimicry' responses. Paradoxically, cancer-initiating events also facilitate transcription of repetitive elements. Contributions of repetitive element transcription towards cancer initiation, and the mechanisms by which cancer cells evade lethal viral mimicry responses during tumor initiation remain poorly understood.
View Article and Find Full Text PDF"Viral mimicry" refers to the induction of an innate immune response and interferon signaling by endogenous stimuli such as double-stranded RNA (dsRNA). This response has been shown to have strong cancer therapeutic potential, including by enhancing the effectiveness of immune checkpoint inhibition (ICI) therapies, and may represent a tumor suppression mechanism that needs to be overcome for malignant transformation to proceed. In a recent study, Zhou and colleagues identify KRAS, a frequently mutated oncogene, as a negative regulator of dsRNA and viral mimicry in an ICI-resistant colorectal cancer model.
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- Absent in melanoma 2 (AIM2) is an important protein that detects foreign DNA from bacteria and viruses, but its role in fighting infections from extracellular bacteria is not well understood.
- Research shows that mice lacking AIM2 are more vulnerable to infections caused by a specific type of bacteria (identified as "pathogenic ."), indicating that AIM2 is crucial for protecting the host.
- The study reveals that AIM2 helps activate inflammasome signaling, which is essential for effectively killing and clearing bacterial infections, particularly through recognizing DNA from these pathogens.
Background & Aims: N6-methyladenosine (mA) governs the fate of RNAs through mA readers. Colorectal cancer (CRC) exhibits aberrant mA modifications and expression of mA regulators. However, how mA readers interpret oncogenic mA methylome to promote malignant transformation remains to be illustrated.
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