Background: Iron metabolism has emerged as a critical factor in cancer biology, with elevated intracellular iron levels contributing to increased oxidative stress and tumorigenesis. However, the molecular determinants governing ferroptosis sensitivity remain incompletely understood. Triosephosphate isomerase 1 (TPI1), a key glycolytic enzyme, has been implicated in cancer progression, but its role in ferroptosis regulation, particularly in the context of chemoresistance, is largely unexplored. In this study, we investigated the impact of TPI1 silencing on ferroptosis in cisplatin-resistant oral squamous cell carcinoma (OSCC), aiming to elucidate its mechanistic role and therapeutic potential. Methods: We conducted in vitro and in vivo analyses to evaluate the functional consequences of TPI1 knockdown in cisplatin-resistant OSCC cell lines and tumor xenograft models. The effects of TPI1 silencing and/or cisplatin treatment were assessed with respect to cell proliferation, migration, and invasion, along with ferroptosis-associated markers, including lipid ROS, free iron levels, lipid peroxidation, and the expression of key ferroptosis-related genes. Additionally, we analyzed the clinical relevance of TPI1 expression in human OSCC tissue samples, examining its association with clinicopathological features and patient prognosis. Results: TPI1 was found to be significantly upregulated in both OSCC tissues and cell lines, and high TPI1 expression correlated with poor clinical outcomes. Multivariate analysis identified TPI1 as an independent prognostic factor for tumor progression. Functionally, TPI1 knockdown suppressed OSCC cell proliferation, migration, and invasion, while its overexpression enhanced these oncogenic behaviors. Mechanistically, silencing TPI1 led to increased intracellular ROS accumulation, elevated free iron, and enhanced lipid peroxidation, collectively promoting ferroptotic cell death in cisplatin-resistant OSCC cells. In vivo, TPI1 depletion resulted in marked tumor growth inhibition and synergized with cisplatin to further suppress tumor burden in xenograft models. Moreover, TPI1 silencing disrupted the epithelial–mesenchymal transition (EMT), a key driver of cancer metastasis and drug resistance. Conclusions: Our study reveals a previously unrecognized role of TPI1 in protecting oral cancer cells from ferroptosis, especially in the setting of cisplatin resistance. These findings suggest that TPI1 not only contributes to tumor aggressiveness but also mediates resistance to ferroptosis. Targeting TPI1 may therefore represent a promising therapeutic strategy to overcome chemoresistance and enhance ferroptosis-based therapies in oral cancer.

This study developed a novel dual-wavelength confocal laser speckle imaging platform. The system includes both visible and near-infrared lasers and two imaging modes: confocal and wide-field laser speckle contrast imaging. The experimental results confirm that the proposed system can be used to measure not only blood flow but also blood oxygen saturation. Additionally, we proposed a blood flow perfusion imaging method called BlingNet (a blood flow imaging CNN) based on the laser speckle contrast imaging technique and deep learning approach. Compared to the traditional nonlinear fitting method, this method has superior accuracy and robustness with higher imaging speed, making real-time blood flow imaging possible.

The time-stretch (TS) imaging system is one type of ultrafast optical imaging system that enables imaging with an unprecedented imaging speed of tens of hundreds of megahertz. The TS imaging achieves linear one-to-one mapping between wavelength and time using a temporal dispersive medium. However, the data issue of high throughput and the fixed resolution in TS imaging limits its wide applications. In this paper, we propose an ultrafast optical imaging system with anamorphic transformation (AT) based on the STEAM structure, which has the benefit of data compression and changing group delay-related resolution. AT is obtained by the usage of chirped fiber Bragg grating (CFBG) with a nonlinear group delay profile. A state-of-the-art experimental demonstration shows that more acquired data are employed to describe the dense information region and the group delay-related resolution is improved by 58% using our proposed ultrafast optical imaging system without reducing the line scanning speed of 50 MHz. The proposal could increase the group delay-related resolution of the target image without adding extra data acquisition or changing the system setup, which has great potential in ultrafast optical imaging systems. Furthermore, the AT in our proposal could also be applied to data compression algorithms to mitigate the data issue in ultrafast optical imaging systems.

Oral squamous cell carcinoma (OSCC) is typified by extensive stromal fibrosis and an immunosuppressive microenvironment, both of which impede effective responses to immune checkpoint blockade. In this study, we identify prolyl 3-hydroxylase family member 4 (P3H4) as a critical mediator of extracellular matrix (ECM) remodeling, epithelial–mesenchymal transition (EMT), and the exclusion of cytotoxic CD8⁺ T lymphocytes. Elevated P3H4 expression correlates with unfavorable clinical outcomes and resistance to immunotherapy. Genetic ablation of P3H4 significantly attenuates tumor progression and promotes CD8⁺ T cell infiltration. To pharmacologically target P3H4, we engineered a liposomal formulation of 1,4-dihydrophenanthroline-2,5-dicarboxylic acid (1,4-DPCA), a small-molecule prolyl hydroxylase inhibitor. This nanomedicine, designated Lipo-1,4-DPCA, effectively downregulates P3H4 expression, mitigates tumor-associated fibrosis, reprograms the immune microenvironment, and elicits robust anti-tumor responses in vivo. Collectively, our findings establish P3H4 as a promising therapeutic target and highlight Lipo-1,4-DPCA as a dual-functional nanotherapeutic candidate capable of enhancing the efficacy of immunotherapy in OSCC.