Lung Cancer

P=N/A, N=220, Active, not recruiting, Medical University of South Carolina | Not yet recruiting --> Active, not recruiting

P1/2, N=296, Active, not recruiting, Inhibrx Biosciences, Inc | Recruiting --> Active, not recruiting

P2, N=21, Recruiting, Mario Negri Institute for Pharmacological Research | Not yet recruiting --> Recruiting

P2, N=40, Active, not recruiting, Shanghai Pulmonary Hospital, Shanghai, China | Not yet recruiting --> Active, not recruiting

P3, N=320, Recruiting, Canadian Cancer Trials Group | Not yet recruiting --> Recruiting

P1/2, N=36, Terminated, SignalChem Lifesciences Corporation | N=92 --> 36 | Trial completion date: Sep 2028 --> Dec 2025 | Recruiting --> Terminated | Trial primary completion date: Sep 2026 --> Dec 2025; Lack of efficacy and enrollment challenges

P3, N=576, Recruiting, Suzhou Suncadia Biopharmaceuticals Co., Ltd. | Not yet recruiting --> Recruiting

Our findings provide novel insights into the heterogeneity of miRNA expression in the pancreas and the molecular mechanisms underlying pancreatic cancer, offering potential targets for future diagnostic and therapeutic strategies.

Collectively, our findings reveal a novel mechanism whereby CD147 promotes crinophagy-mediated exosome secretion through dual regulation of GCN2 stability and calcium homeostasis, thereby accelerating NSCLC progression. Our work establishes a new molecular link between autophagy modulation and cancer progression.

Furthermore, we discovered that triptolide (TPL), an HNF1A inhibitor, impeded HHIPL2-mediated Sonic Hedgehog signaling activation and NSCLC malignancy. Therefore, our findings not only uncover a previously unrecognized role for HHIPL2 in regulating the Sonic Hedgehog signaling pathway but also highlight a novel HHIPL2/HNRNPC/HNF1A axis as an attractive target for NSCLC therapy.Schematic diagram (created by Figdraw.com) showing that HHIPL2 positively governs Hedgehog signaling to accelerate NSCLC progression via enhancing HNRNPC-mediated HNF1A mRNA stabilization.

Importantly, inactivation of the necroptosis executioner MLKL reverses pre-tumoral inflammation, decreases metastasis as well as neuronal-like reprogramming. Taken together, our findings suggest that pre-tumoral inflammatory cell death contributes to neuronal progenitor mimicry, immunosuppression and increased metastasis in SCLC.

Therefore, blockade of CD47 expression attenuated lung cancer growth through suppressing Nrf2 and subsequently increasing the expression of FPN. CD47 exerts immune evasion via Nrf2/FPN axis.