Sciellin promotes the development and progression of thyroid cancer through the JAK2/STAT3 signaling pathway.

Thyroid cancer (TC) is one of the most common endocrine tumors worldwide. Sciellin (SCEL) is involved in various disease processes, including burn wound healing and neutrophil extracellular traps (NETs); it is highly expressed in TC. However, its biological impact on TC and related mechanisms remain unclear. This study aimed to investigate the effect of SCEL on the function of human TC cell lines B-CPAP and OCUT-2C (cancer cell lines with BRAF V600E mutations). Analyses of data sets and clinical samples revealed enhanced expression of SCEL in TC than in adjacent normal tissue. SCEL knockout suppresses proliferation and cell cycle progression in TC cells, and these results were reversed by the upregulated SCEL expression in TC. SCEL knockout inhibited tumor development in xenograft mouse models. Western blot (WB) demonstrated that the expression of p-JAK2 and p-STAT3 was reduced in SCEL-knockdown TC. These results suggest that SCEL plays a key role in TC progression through the JAK2-STAT3 pathway. Therefore, SCEL can be considered a potential diagnostic biomarker and therapeutic target for TC.

Ibuprofen inhibits anaplastic thyroid cells in vivo and in vitro by triggering NLRP3-ASC-GSDMD-dependent pyroptosis.

Pyroptosis is a novel type of proinflammatory programmed cell death that is associated with inflammation, immunity, and cancer. Anaplastic thyroid carcinoma (ATC) has a high fatality rate, and there is no effective or standard treatment. The disease progresses rapidly and these tumors can invade the trachea and esophagus, leading to breathing and swallowing difficulties. Hence, new treatment methods are greatly needed. Ibuprofen is a common drug that can exert antitumor effects in some cancers. In this study, we demonstrated in vitro and in vivo that ibuprofen can induce ATC pyroptosis. Hence, we treated C643 and OCUT-2C ATC cells with ibuprofen and found that several dying cells presented the characteristic morphological features of pyroptosis, such as bubble-like swelling and membrane rupture, accompanied by activation of ASC and NLRP3 and cleavage of GSDMD. Along with the increased release of LDH, ibuprofen treatment promoted apoptosis and inhibited viability, invasion, and migration. However, overexpression of GSDMD significantly inhibited ibuprofen-induced pyroptosis. In vivo, research has demonstrated that thyroid tumor growth in nude mice can be suppressed by ibuprofen-induced pyroptosis in a dose-dependent manner. In this research, we explored a new mechanism by which ibuprofen inhibits ATC growth and progression and highlighted its promise as a therapeutic agent for ATC.

Upregulated SLC27A2/FATP2 in differentiated thyroid carcinoma promotes tumor proliferation and migration.

BACKGROUND: Differentiated thyroid carcinoma (DTC) accounts for the vast majority of thyroid cancer (TC) cases. The rapidly increasing incidence of TC requires the urgent identification of new diagnostic and therapeutic targets. Solute carrier family 27 member 2 (SLC27A2/FATP2) plays an essential role in lipid biosynthesis and fatty acid transport. Recent studies have confirmed its involvement in a variety of diseases, including cancer. METHODS: In this study, the expression of SLC27A2 was analyzed in cancer and paracancerous tissue samples from 98 thyroid cancer patients, and we performed ROC analysis to confirm the diagnostic value. CCK8, Transwell, and other methods were used to study its effect on DTC, and the mechanism of SLC27A2 was investigated by RNA sequencing and Western blot. RESULTS: The expression of SLC27A2 was upregulated in both DTC tissues and cell lines and was correlated with clinical progression. In vitro studies further confirmed that SLC27A2 knockdown attenuated the proliferation and invasion of DTC cells. Through RNA sequence analysis and gene set enrichment analysis, we found that the MAPK pathway is the main downstream signaling pathway for the regulation by SLC27A2. SLC27A2 affects cell proliferation and differentiation by inducing changes in the proto-oncogene C-FOS. CONCLUSIONS: Our results show that SLC27A2 plays an important role in tumor proliferation and migration, providing a new putative target for the diagnosis and treatment of TC.