Summary Drought is an abiotic stress that affects plant growth, and lipids are the main economic factor in the agricultural production of oil crops. However, the molecular mechanisms of drought response function in lipid metabolism remain little known. In this study, overexpression (OE) of different copies of the drought response genes LEA3 and VOC enhanced both drought tolerance and oil content in Brassica napus and Arabidopsis. Meanwhile, seed size, membrane stability and seed weight were also improved in OE lines. In contrast, oil content and drought tolerance were decreased in the AtLEA3 mutant (atlea3) and AtVOC‐RNAi of Arabidopsis and in both BnLEA‐RNAi and BnVOC‐RNAi B. napus RNAi lines. Hybrids between two lines with increased or reduced expression (LEA3‐OE with VOC‐OE, atlea3 with AtVOC‐RNAi) showed corresponding stronger trends in drought tolerance and lipid metabolism. Comparative transcriptomic analysis revealed the mechanisms of drought response gene function in lipid accumulation and drought tolerance. Gene networks involved in fatty acid (FA) synthesis and FA degradation were up‐ and down‐regulated in OE lines, respectively. Key genes in the photosynthetic system and reactive oxygen species (ROS) metabolism were up‐regulated in OE lines and down‐regulated in atlea3 and AtVOC‐RNAi lines, including LACS9, LIPASE1, PSAN, LOX2 and SOD1. Further analysis of photosynthetic and ROS enzymatic activities confirmed that the drought response genes LEA3 and VOC altered lipid accumulation mainly via enhancing photosynthetic efficiency and reducing ROS. The present study provides a novel way to improve lipid accumulation in plants, especially in oil production crops.

MYH9 encodes the heavy chain of nonmuscle myosin IIA, a ubiquitously expressed cytoplasmic myosin that regulates the actin cytoskeleton, cell migration, cell polarization, and signal transduction in cancer cells. Here, we investigated the role of MYH9 in cancer stem cells (CSCs) associated with esophageal cancer (EC). The subcellular localization of MYH9 was investigated in SKGT-4 cells through immunofluorescent analysis. MYH9+ and MYH9− spheroid cells were derived from SKGT-4 cells by flow cytometry and compared for self-renewal capacity, tumorigenicity, CD133 positivity, cisplatin resistance, and phosphatidylinositol-3kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) activity. MYH9 messenger RNA expression was assessed in 30 EC patients by quantitative reverse transcription-polymerase chain reaction. Kaplan-Meier curves were plotted to explore the influence of MYH9 on EC survival. MYH9 localized to the plasma membrane, cytoplasm, and nucleus of SKGT-4 cells. Spheroid cells displayed higher MYH9 expression and positivity compared to parental SKGT-4 cells. MYH9+ cells showed strong CSC characteristics, including in vivo tumorigenicity, migration, invasion, cisplatin resistance, and CD133+ positivity. MYH9 activated the PI3K/ AKT/mTOR axis in CSCs and was upregulated in EC patients with poor survival. Collectively, these data show that MYH9 significantly promotes tumorigenesis by regulating PI3K/AKT/mTOR signaling in EC. MYH9 expression remarkably correlates with poor prognosis and represents a novel biomarker and drug target for the diagnosis and treatment of EC.

Mullerian cysts are benign tumors that are very rare in the posterior mediastinum. It is necessary to distinguish Mullerian cysts from benign tumors or other types of cyst in the posterior mediastinum. A 42-year-old woman visited our hospital for a routine check-up, and a mediastinal mass was identified on chest computed tomography (CT). Contrast-enhanced chest magnetic resonance imaging (MRI) revealed a 4.0 × 2.6 × 2.8-cm mass, and a neurogenic tumor or esophageal cyst was suspected. Single-port thoracoscopic surgery was performed for cyst removal. Histopathological examination of the resected tissue revealed that the cyst wall was covered with a single layer of ciliated columnar epithelium. Immunohistochemical staining revealed positivity for paired box gene 8 (PAX8), Wilms tumor protein 1 (WT-1), estrogen receptor (ER), and progesterone receptor (PR). Therefore, a diagnosis of mediastinal Mullerian cyst was made. Mediastinal Mullerian cysts should be included in the differential diagnosis of posterior mediastinal cysts. Cystic lesions in the posterior mediastinum should be removed surgically and undergo immunohistochemical examination.