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Supportinginformation and the ORCID identification number(s) for the author(s) of this article can be found under: https://doi.

This study shows lithosphere evolution history in the west North China Craton (NCC) from the early Cretaceous to Quaternary by studying the major element, trace element and Sr-Nd-Hf isotope compositions in Jining basalts of 119.6108.6 Ma, 23.521.9 Ma and 1.30.11 Ma.The early Cretaceous basalts (119.6108.6 Ma) display enriched characteristics with high contents of incompatible elements, high 87 Sr/ 86 Sr i , low ε Nd (t) and low ε Hf (t). These basalts resulted from partial melting of ancient metasomatized lithospheric mantle, and we consider the 119.6108.6 Ma magmatism as indicating lithosphere thinning in the west NCC. Although the Pacific slab seen seismically in the mantle transition zone beneath eastern China is no older than 60 Ma, there exists convincing evidence for the presence of the Paleo-Pacific slab in the transition-zone in the Mesozoic. Thus we propose that the water released from the transition-zone slab hydrated A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPTthe overlying lithosphere and further converted the base of the lithosphere into asthenosphere. This is the most likely mechanism responsible for the lithosphere thinning in the west NCC and the petrogenesis of the Jining 119.6108.6 Ma basalts. Sr i , high ε Nd (t) and high ε Hf (t). Upwelling and decompression melting of the eastward flowing asthenosphere from beneath western plateaus to beneath eastern hilly plains in the Cenozoic is the most plausible mechanism for the petrogenesis of Jining Cenozoic basalts (both of 23.521.9 Ma and 1.30.11 Ma), but the Jining 1.30.11 Ma basalts must have been produced beneath even thinner lithosphere.Taken together geophysical studies and our petrological and geochemical studies of all these three episodes of the Jining basalts, wepropose that the lithosphere in the west NCC has been thinning since the early Cretaceous and the thinning continues to the present.

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Background Transfer of noncoding microRNAs (miRNAs) by extracellular vesicles (EVs) promotes the development of chemoresistance in many tumor types. Additionally, restoration or depletion of several miRNAs has been observed in multiple cancer types including gastric cancer (GC). In this present study, we aimed to investigate the mechanism of miR-130b-3p in M2 macrophage-derived EVs in the development of GC through regulation of mixed lineage leukemia 3 (MLL3) and grainyhead-like 2 (GRHL2). Methods Expression of miR-130b-3p and GRHL2 was quantified in 63 pairs of cancerous and noncancerous gastric tissues. The predicted binding between miR-130b-3p and MLL3, together with the enrichment of MLL3, H3K4me1, and H3K27ac in gene enhancer region, was verified by luciferase activity assay and chromatin immunoprecipitation. Effects of miR-130b-3p on GC cell proliferation, apoptosis, migration and invasion, as well as tube formation of human umbilical endothelial vein cells (HUEVCs) were further determined by gain- and loss-of function assays in vitro. Results miR-130b-3p was upregulated in GC tissues, and miR-130b-3p promoted survival, metastasis and angiogenesis of GC cells as well as enhanced tumor formation and angiogenesis in GC in vivo. Additionally, miR-130b-3p delivered in M2 macrophage-derived EVs promoted survival, migration, invasion, and angiogenesis of GC cells. Notably, MLL3 inhibited GC cell proliferation, migration, invasion, and vessel-like tube formation of HUEVCs by increasing GRHL2. Furthermore, downregulation of miR-130b-3p in M2 macrophage-derived EVs or upregulation of GRHL2 inhibited tumor formation and angiogenesis in GC. Conclusion This study highlights that EVs loaded with the specific miRNA cargo miR-130b-3p mediate communication between M2 macrophages and cancer cells in the tumor microenvironment through the modulation of MLL3 and GRHL2 in GC.