ALBERT

Description: Galectin-3 is a ubiquitous lectin exerting multiple cellular functions such as RNA splicing, protein trafficking and apoptosis. Its expression is positively correlated with the poor prognosis in lung cancer patients. Galectin-3 can promote cancer progression through its effects on cell proliferation, cell survival or cancer metastasis. However, the role of galectin-3 in the regulation of cancer stem-like cells (CSCs) is still unclear. Here, we investigated the hypothesis that galectin-3 might regulate lung CSCs via the EGF receptor (EGFR) signaling pathway. In our study, galectin-3 facilitated EGFR activation and enhanced the sphere formation activity of lung cancer cells. Furthermore, galectin-3 promoted Sox2 expression in an EGFR activation-dependent manner; importantly, forced expression of Sox2 blunted the effect of galectin-3 knockdown on lung cancer sphere formation ability. These results suggest that galectin-3 promotes EGFR activation leading to the upregulation of Sox2 expression and lung CSCs properties. Moreover, we showed that the carbohydrate-binding activity of galectin-3 was important for the regulation of EGFR activation, Sox2 expression and sphere formation. We have recently reported that c-Myc is a transcriptional activator of Sox2. We further found that galectin-3 enhanced c-Myc protein stability leading to increased c-Myc binding to the Sox2 gene promoter. We also examined the effect of the stemness factors, Oct4, Nanog and Sox2 on the expression of galectin-3. We found that Oct4 enhanced galectin-3 expression. Our results together suggest that galectin-3 enhances lung cancer stemness through the EGFR/c-Myc/Sox2 axis; Oct4, in turn, promotes galectin-3 expression, forming a positive regulatory loop in lung CSCs.

Description: During arc-continent collision, buoyant sections of sediments and rifted continental crust from a subducting plate will accrete to the forearc of the upper plate as long as this backstop remains intact. Deformation of the oceanic arc and forearc block may ultimately lead to accretion of these mafic rock units to the new orogen. The Taiwan mountain belt, which formed at ~6.5 Ma by oblique convergence between the Eurasian passive margin and the overriding Luzon arc in northern Taiwan, offers important insight in this process, since the collision is more advanced in the north than in the south. The incipient stage of arc-collision can be studied in southern Taiwan, while the northern portion of the orogen is presently undergoing collapse due to a flip in the subduction polarity between the Eurasian Plate and the Philippine Sea Plate. In this study, we seismically image the structure of the northern section of the mountain belt with a tomographic inversion. We present marine and land-based seismic refraction data, as well as local earthquake data, from transect T6 of the Taiwan Integrated Geodynamic Research (TAIGER) program across the Taiwan mountain belt and the adjacent Ryukyu arc. Our 2-D compressional seismic velocity model for this transect, which is based on a tomographic inversion of 10 213 P -wave arrival times, shows that the Eurasian crystalline continental crust thickens from ~24 km in the Taiwan Strait to ~40 km beneath the eastern Central Range of Taiwan. The detailed seismic velocity structure of the Taiwan mountain belt shows vertical continuity in the upper 15 km, which suggests that rocks are exhumed to the surface here from the middle crust in a near-vertical path. The continental crust of the westernmost Ryukyu arc is almost as thick (~40 km) as in the adjacent northern Central Range of Taiwan, and it appears to override the leading edge of the Philippine Sea Plate offshore northeastern Taiwan. If we assume that the western Ryukyu arc crust also thickened in the collision, then the mountain belt is wider and less thick in northern Taiwan than in central Taiwan (~50 km), which may be the result of post-collisional extension in the north.

Description: Gene regulation change has long been recognized as an important mechanism for phenotypic evolution. We used the evolution of yeast aerobic fermentation as a model to explore how gene regulation has evolved and how this process has contributed to phenotypic evolution and adaptation. Most eukaryotes fully oxidize glucose to CO 2 and H 2 O in mitochondria to maximize energy yield, whereas some yeasts, such as Saccharomyces cerevisiae and its relatives, predominantly ferment glucose into ethanol even in the presence of oxygen, a phenomenon known as aerobic fermentation. We examined the genome-wide gene expression levels among 12 different yeasts and found that a group of genes involved in the mitochondrial respiration process showed the largest reduction in gene expression level during the evolution of aerobic fermentation. Our analysis revealed that the downregulation of these genes was significantly associated with massive loss of binding motifs of Cbf1p in the fermentative yeasts. Our experimental assays confirmed the binding of Cbf1p to the predicted motif and the activator role of Cbf1p. In summary, our study laid a foundation to unravel the long-time mystery about the genetic basis of evolution of aerobic fermentation, providing new insights into understanding the role of cis -regulatory changes in phenotypic evolution.