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Abstract Nonprogrammed cell death (NPCD) and programmed cell death (PCD) are two types of cell death. Cell death is significantly linked to tumor development, medication resistance, cancer recurrence, and metastatic dissemination. Therefore, a comprehensive understanding of cell death is essential for the treatment of cancer. Pyroptosis is a kind of PCD distinct from autophagy and apoptosis in terms of the structure and function of cells. The defining features of pyroptosis include the release of an inflammatory cascade reaction and the expulsion of lysosomes, inflammatory mediators, and other cellular substances from within the cell. Additionally, it displays variations in osmotic pressure both within and outside the cell. Pyroptosis, as evidenced by a growing body of research, is critical for controlling the development of inflammatory diseases and cancer. In this paper, we reviewed the current level of knowledge on the mechanism of pyroptosis and inflammasomes and their connection to cancer and inflammatory diseases. This article presents a theoretical framework for investigating the potential of therapeutic targets in cancer and inflammatory diseases, overcoming medication resistance, establishing nanomedicines associated with pyroptosis, and developing risk prediction models in refractory cancer. Given the link between pyroptosis and the emergence of cancer and inflammatory diseases, pyroptosis‐targeted treatments may be a cutting‐edge treatment strategy.

Background: During tumor formation and expansion, increasing glucose metabolism is necessary for unrestricted growth of tumor cells. Expression of key glycolytic enzyme alpha-enolase (ENO1) is controversial and its modulatory mechanisms are still unclear in non-small cell lung cancer (NSCLC). Methods: The expression of ENO1 was examined in NSCLC and non-cancerous lung tissues, NSCLC cell lines, and immortalized human bronchial epithelial cell (HBE) by quantitative real-time reverse transcription PCR (qRT-PCR), immunohistochemistry, and Western blot, respectively. The effects and modulatory mechanisms of ENO1 on cell glycolysis, growth, migration, invasion, and in vivo tumorigenesis and metastasis in nude mice were also analyzed. Results: ENO1 expression was increased in NSCLC tissues in comparison to non-cancerous lung tissues. Similarly, NSCLC cell lines A549 and SPCA-1 also express higher ENO1 than HBE cell line in both mRNA and protein levels. Overexpressed ENO1 significantly elevated NSCLC cell glycolysis, proliferation, clone formation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo by regulating the expression of glycolysis, cell cycle, and epithelial-mesenchymal transition (EMT)-associated genes. Conversely, ENO1 knockdown reversed these effects. More importantly, our further study revealed that stably upregulated ENO1 activated FAK/PI3K/AKT and its downstream signals to regulate the glycolysis, cell cycle, and EMT-associated genes. Conclusion: This study showed that ENO1 is responsible for NSCLC proliferation and metastasis; thus, ENO1 might serve as a potential molecular therapeutic target for NSCLC treatment. [ABSTRACT FROM AUTHOR]

Patients with oral cancer often have to undergo the surgery for mandibular excision. Once the bone in the cancerous area is removed, not only the facial area but also chewing function of the patient is needed to be repaired by clinicians. In recent years, the rapid growth of three-dimensional (3D) metal printing technology has meant that higher-quality facial reconstructions are now possible, which could even restore chewing function. This study developed 3D-printed titanium (Ti)-alloy reconstruction implant for a prosthesis designed for mandibular segmental osteotomy defects, and 3D finite element (FE) analysis was conducted to evaluate its biomechanical performance. The analyzed parameters in the FE models were as follows: (1) two prosthesis designs, namely a prosthesis retaining the residual mandibular bone (for patients with mild oral cancer) and a prosthesis with complete mandibular resection (for patients with severe oral cancer); (2) two lengths of prosthesis, namely 20 and 25 mm; and (3) three thicknesses of prosthesis, namely 0.8, 1, and 1.5 mm. A 45° lateral bite force (100 N) was applied to the top of the prosthesis as the loading condition. The results revealed that for the two prosthesis designs, the prosthesis retaining the residual mandibular bone showed higher stress on the prosthesis and cortical bone compared with the prosthesis with complete mandibular resection. Regarding the two prosthesis lengths, no fixed trend of prosthesis stress was found, but stress in the cortical bone was relatively high for a prosthesis length of 20 mm compared with that of 25 mm. For the three prosthesis thicknesses, as the thickness of the prosthesis decreased, the stress in the prosthesis decreased but the stress in the cortical bone increased. These findings require confirmation in future clinical investigations.