LIN28B (Lin-28 Homolog B)

In a Huh-7 xenograft tumor model, pre-let-7-PROTACs exhibited significant synergistic antitumor effects when combined with sorafenib (SFB). This study confirmed that pre-let-7-PROTACs reduce tumor stemness by degrading Lin28B, offering a promising therapeutic approach for HCC.

Our laboratory recently identified the actin-binding protein advillin (AVIL) as being overexpressed, oncogenic, and necessary for tumorigenesis in GBM. Here, we further examined AVIL expression in GBMs and found that it was enriched across molecular subtypes and states, including GBM stem cells and temozolomide-resistant samples...In summary, we have identified an efficacious first-in-class compound targeting an oncogene in GBM. Further optimization of the molecule may offer an effective therapeutic intervention for GBM.

We develop a targeted siRNA nanoparticle delivery system (siLin28B/DSSP@lip-PEG-FA) in combination with the PARP inhibitor BMN673, providing a synergistic therapeutic strategy against MSE...Furthermore, in vitro and in vivo experiments demonstrated that suppression of PARP and LIN28B inhibited vascular leakage and reinforced tight junction integrity. Collectively, our findings highlight dual targeting of PARP and LIN28B as a promising MA management approach in patients with advanced cancers, with the potential to improve patient quality of life.

Lin28b promotes a substantial increase in lipid content, upon which the survival of Rpl22-deficient leukemias depends. Altogether, these findings reveal that Rpl22 insufficiency enhances the leukemia potential of HSCs through regulation of FAO and promotes leukemogenesis through Lin28b promotion of lipid synthesis.

In animal models and clinical tissues, NRAV expression correlates with disease progression and CSC marker accumulation. Our findings uncover a novel NRAV-let-7c-5p-LIN28B axis that links m6A modification to CSC maintenance in HCC, highlighting a potential therapeutic target for disrupting stemness pathways in liver cancer.

Furthermore, CERS6-AS1 depletion similarly attenuated malignant phenotypes, effects that were rescued by LIN28B overexpression. Collectively, the CERS6-AS1-regulated IGF2BP1/LIN28B signaling axis promoted ovarian cancer progression by enhancing tumor cell proliferation, migration and invasion, highlighting this pathway as a promising therapeutic target.

Our findings highlight the potential clinical utility of C1orf112 as a diagnostic and prognostic biomarker in EC, and provide new insights into its regulatory molecular network. This study proposes a conceptual framework for understanding EC pathogenesis and guiding the development of targeted therapies. Nonetheless, further prospective clinical studies and mechanistic investigations are warranted to validate these findings.

HAD/ACED demonstrated higher TP53 mutation accumulation and TP53-related cancer stemness gene overexpression, including LIN28B, IGF2BP1, and HMGA2. Therefore, TP53 and these cancer stemness genes might be involved in the occurrence of HAD/ACED.

Screening for factors that activated luciferase reporters of the human LIN28A and LIN28B promoters, in combination with genetic mouse models, we demonstrate positive feedforward loops between key developmental transcription factors such as B-Catenin, Sox2, Sox9, and Lin28-RBPs. Furthermore, we demonstrate heterochronic regulation of morphogenesis is not only genetically modulated but also molecularly fine-tuned via position-dependent sequences in the 5' and/or 3' untranslated regions.

Our findings suggest that this four-gene panel holds significant promise as a robust prognostic tool for breast cancer survival. This research paves the way for further investigations into targeted therapies and personalized medicine approaches in the management of breast cancer.

LIN28B activation via promoter hypomethylation defines a high-risk JMML subgroup with cell cycle. Methylation-based stratification predicts survival, positioning LIN28B as a therapeutic target.

We constructed and validated a robust signature of six lncRNA CASC for predicting survival of CRC patients and characterizing the immune infiltration landscape. These results reveal that the CASC gene family could be a therapeutic target for CRC patients.