As a postdoctoral researcher based in Hong Kong, participating in the Hong Kong Laureate Forum (HKLF) offers unparalleled opportunities to deepen local academic collaborations while efficiently expanding my professional network. My previous HKLF experience profoundly enriched my research journey: I gained insights from leading experts in my field, connected with global peers—many of whom remain valuable contacts today—and resolved technical challenges through lab visits at Hong Kong institutions. These interactions not only advanced my work but also cultivated lasting friendships, with ongoing exchanges about career developments and cross-cultural experiences.

Moreover, despite living here for six years during my PhD, HKLF’s curated tours of museums and landmarks deepened my appreciation for Hong Kong’s unique culture, solidifying my commitment to contribute long-term to this dynamic city. Now, as a more experienced researcher, I am eager to leverage my expertise to engage in meaningful dialogues, explore collaborative projects, and mentor early-career scholars.

The forum’s blend of intellectual rigor and cultural immersion aligns perfectly with my goals to strengthen both academic and community ties in Hong Kong. I am confident that my proactive participation will enrich discussions while further integrating me into this vibrant hub of innovation.

Thank you for considering my application.

The Curious Case of Benjamin Button in Glioblastoma: A Switch of Aging and Immune Evasion Controlled by a Novel MSI1 Phosphorylation

This study uncovers a phosphorylation-dependent mechanism by which Musashi-1 (MSI1) orchestrates glioblastoma (GBM) progression through senescence suppression and immune evasion. While cellular senescence enhances tumor surveillance, MSI1 paradoxically drives GBM malignancy. Using CRISPR-edited GBM cell lines, orthotopic mouse models, and 35 patient-derived tissues, we identified a novel phosphorylation site at MSI1-Serine 347 (S347) linked to poor survival. A custom antibody revealed elevated phosphorylated MSI1 (p-MSI1) in GBM versus normal tissues. Functional studies demonstrated that S347 phosphorylation loss (S347A mutant) induced p21-mediated cell cycle arrest and senescence, while transcriptomics highlighted immune pathway enrichment. Specifically, IL-21 receptor (IL21R) emerged as a hub gene in immune response and membrane signaling, with MAPK activation linked to the S347 phosphorylation state, suggesting an IL21R-MAPK axis in senescence-associated immune evasion.

These findings establish MSI1-S347 phosphorylation as a dual regulator: suppressing senescence via p21 and promoting immune escape through MAPK signaling. Clinically, p-MSI1 serves as a prognostic biomarker and therapeutic target. We propose combinatorial strategies to exploit this pathway, including senescence induction (CDK4/6 inhibitors + S347 decoy peptides) and MAPK modulation to reverse immune suppression.