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7. STK11 (LKB1) mutation suppresses ferroptosis in lung adenocarcinoma by facilitating monounsaturated fatty acid synthesis

Author

Zou Qiang, Tang Bo, Chen Xianchao, Zhang Chuang, and Huang Yun

Subjects
stk11, lung adenocarcinoma, monounsaturated fatty acid synthesis, ferroptosis, Medicine
Abstract

Serine/threonine kinase 11 (STK11), a tumor suppressor gene, exhibits frequent mutations in lung adenocarcinoma (LUAD). However, the specific molecular mechanisms by which STK11 mutations exert an influence on the biosynthesis of monounsaturated fatty acids (MUFAs) and subsequently affect ferroptosis in LUAD remain indistinct. In this study, bioinformatic analysis was employed to probe into the linkage between STK11 and key inhibitory genes of ferroptosis, namely SLC7A11 and SCD1, in LUAD tissues. Quantitative reverse transcription polymerase chain reaction was employed to assess the expression of STK11 in both wild-type and mutant STK11 LUAD cells, cell counting kit-8 to assess cell viability, and flow cytometry to detect apoptosis. A transmission electron microscope was utilized to observe mitochondrial morphology, and Western blot to ascertain the protein expression of STK11, ferroptosis-related proteins, and the enzyme SCD1 involved in MUFA synthesis. Oil red O staining was employed to test the distribution of lipid droplets in cancer cells, and a lipid quantification method to measure the content of MUFAs. Commercial kits were employed to assess the levels of lipid reactive oxygen species, malondialdehyde, glutathione, and Fe2+ in cells. The result revealed a negative correlation between STK11 and SLC7A11 as well as SCD1, with STK11 expression downregulated in mutant STK11 LUAD cells. Furthermore, STK11 mutations were found to suppress ferroptosis in LUAD cells by affecting MUFA synthesis. Subsequent rescue assays demonstrated that STK11 mutations hindered ferroptosis by impacting the synthesis of MUFAs in LUAD cells. This study provided evidence that STK11 mutations suppressed ferroptosis in LUAD cells by promoting MUFA synthesis, thus offering a novel research direction in the management of LUAD.

Published
2024
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26. USP47 inhibits [m.sup.6]A-dependent c-Myc translation to maintain regulatory T cell metabolic and functional homeostasis

Author

Wang, Aiting, Huang, Haiyan, Shi, Jian-Hong, Yu, Xiaoyan, Ding, Rui, Zhang, Yuerong, Han, Qiaoqiao, Ni, Zhi-Yu, Li, Xia, Zhao, Ren, and Zou, Qiang

Subjects
T cells -- Physiological aspects, Genetic translation -- Physiological aspects, Homeostasis -- Physiological aspects, Immune response -- Physiological aspects, Colorectal cancer -- Development and progression, Immunotherapy -- Physiological aspects, Ubiquitin -- Physiological aspects, Stomach cancer -- Development and progression, RNA -- Physiological aspects, Health care industry
Abstract

The functional integrity of Tregs is interwoven with cellular metabolism; however, the mechanisms governing Treg metabolic programs remain elusive. Here, we identified that the deubiquitinase USP47 inhibited c-Myc translation mediated by the RNA [N.sup.6]-methyladenosine ([m.sup.6]A) reader YTHDF1 to maintain Treg metabolic and functional homeostasis. USP47 positively correlated with the tumor-infiltrating Treg signature in samples from patients with colorectal cancer and gastric cancer. USP47 ablation compromised Treg homeostasis and function in vivo, resulting in the development of inflammatory disorders, and boosted antitumor immune responses. USP47 deficiency in Tregs triggered the accumulation of the c-Myc protein and in turn exacerbated hyperglycolysis. Mechanistically, USP47 prevented YTHDF1 ubiquitination to attenuate the association of YTHDF1 with translation initiation machinery, thereby decreasing [m.sup.6]A-based c-Myc translation efficiency. Our findings reveal that USP47 directs [m.sup.6]A-dependent metabolic programs to orchestrate Treg homeostasis and suggest novel approaches for selective immune modulation in cancer and autoimmune diseases by targeting of USP47., Introduction Tregs are essential for immune tolerance and play a critical role in preventing autoimmune inflammation and associated pathologies (1-3). Tregs also drive immunosuppression to dampen antitumor immune responses in [...]

Published
2023
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