Hepatocellular Cancer

P=N/A, N=100, Recruiting, Tata Memorial Centre

P1, N=149, Active, not recruiting, Boehringer Ingelheim | Recruiting --> Active, not recruiting | Trial completion date: May 2028 --> Feb 2028

P1, N=30, Active, not recruiting, Tianjin Medical University Cancer Institute and Hospital | Recruiting --> Active, not recruiting | Trial completion date: Nov 2025 --> Nov 2026

Our findings identifies a distinct mechanism whereby activated HSCs transfer LDs to hepatic macrophages, inducing M2 polarization and creating a pro-tumorigenic microenvironment. This HSC-macrophage crosstalk represents a potential metabolic therapeutic target for preventing HCC development in patients with chronic liver disease.

In addition, Exo-miR-488-3p tended to induce HepG2 cells apoptosis, though this relationship was not statistically significant. In conclusion, exo-miR-488-3p inhibits the malignant cytological activities in HCC, a possible strategy in the treatment of HCC.

This study provides an exploratory overview of somatic alterations detected by a targeted sequencing panel in a regional HCC cohort. Given the limitations inherent to panel-based analyses and the lack of independent validation, these findings should be interpreted cautiously and primarily serve as a reference for future large-scale and experimentally validated studies aimed at refining precision oncology strategies in HCC.

Overexpression of RBM15B or KDM4C attenuated ferroptosis and reversed the suppression of HCC cell growth induced by FOXP2 overexpression. In conclusion, FOXP2 may promote ferroptosis and inhibit cell proliferation in HCC by decreasing SLC7A11 expression via the RBM15B/KDM4C axis in an m6A-dependent manner.

MFN2 inhibits HSC activation and liver fibrosis by suppressing β-catenin nuclear translocation, making it a promising therapeutic target for NAFLD-related fibrosis and associated complications, such as hepatocellular carcinoma.

Furthermore, this article also explores the potential of combination therapies, including targeting HSPs/HIF-1α, reversing immunosuppression, eliminating cancer stem cells (CSCs), and intervening in CAFs. This study provides a solid theoretical foundation for addressing the challenge of HCC recurrence, holding significant importance for improving patient prognosis and guiding clinical translation.

C5aR1 deficiency or depletion of CD8+ T cells hinders the anti-HCC effects of citalopram. Collectively, our study reveals the immunomodulatory roles of citalopram in inducing anti-tumor immunity and provides a basis for considering the repurposing of SSRIs as promising anticancer agents for HCC treatment.

Drug sensitivity analysis revealed higher sensitivity to chemotherapeutic agents in high-risk patients. Integrated transcriptomics establishes aberrant sialylation as a key LIHC prognostic biomarker and therapeutic target by stratifying risk subgroups and revealing immunosuppressive microenvironment alterations.