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Understanding the trend characteristics of design rainstorm and spatial heterogeneity of extreme precipitation is of great importance to reduce disasters induced by rare extreme precipitation. Using a high-resolution (0.5° × 0.5°) daily gridded data set of precipitation across mainland China from 1961 to 2013, this study investigated the historical changing trend and spatial heterogeneity of design rainstorm using the 30-year moving window method (30YM). Differences in the quantification of the design rainstorm were compared for the use of the 30YM and the 30-year-based increasing window method (30YBI). The results show that a significant increasing intensity but no spatially uniform trend of design rainstorm can be observed across mainland China based on the 30YM analysis. The south, east, and northeast China mainly showed an increasing trend, but the southwest and north China presented a decreasing trend. The spatial heterogeneity of the design rainstorm was greatly enhanced if the nonstationarity assumption was adopted on the national scale. The heterogeneity showed an increasing trend mainly in southeast, north, northeast, and northwest China, and a decreasing trend in southwest and west China, indicating significant regional variation in spatial heterogeneity. For most areas of mainland China, especially for southeastern, northeastern, and western China, use of the most recent precipitation sub-series to quantify the design rainstorm may weaken the potential nonstationarity and guarantee the safety of infrastructure in these areas where design rainfall increases. [ABSTRACT FROM AUTHOR]

Currently, more than 170 modifications have been identified on RNA. Among these RNA modifications, various methylations account for two-thirds of total cases and exist on almost all RNAs. Roles of RNA modifications in cancer are garnering increasing interest. The research on m6A RNA methylation in cancer is in full swing at present. However, there are still many other popular RNA modifications involved in the regulation of gene expression post-transcriptionally besides m6A RNA methylation. In this review, we focus on several important RNA modifications including m1A, m5C, m7G, 2′-O-Me, Ψ and A-to-I editing in cancer, which will provide a new perspective on tumourigenesis by peeking into the complex regulatory network of epigenetic RNA modifications, transcript processing, and protein translation. [ABSTRACT FROM AUTHOR]

Alternative splicing (AS) is a key process in which precursor RNAs produce different mature RNAs, and the disorder of AS is a key factor in promoting cancer development. Compared with coding RNA, studies on the functions of long non-coding RNAs (lncRNAs) are far from enough. In fact, lncRNA is an important participant and regulator in the process of AS. On the one hand, lncRNAs regulate cancer progression as AS products of precursor messenger RNA (mRNA), but on the other hand, precursor lncRNA generates cancer-related abnormal splicing variants through AS. In addition, lncRNAs directly or indirectly regulate the AS events of downstream target genes, thus affecting the occurrence and development of cancer. Here, we reviewed how lncRNAs regulate AS and influence oncogenesis in different ways. [ABSTRACT FROM AUTHOR]

The successful treatment of human cancers by immunotherapy has been made possible by breakthroughs in the discovery of immune checkpoint regulators, including CTLA-4 and PD-1/PD-L1. However, the immunosuppressive effect of the tumor microenvironment still represents an important bottleneck that limits the success of immunotherapeutic approaches. The tumor microenvironment influences the metabolic crosstalk between tumor cells and tumor-infiltrating immune cells, creating competition for the utilization of nutrients and promoting immunosuppression. In addition, tumor-derived metabolites regulate the activation and effector function of immune cells through a variety of mechanisms; in turn, the metabolites and other factors secreted by immune cells can also become accomplices to cancer development. Immune-metabolic checkpoint regulation is an emerging concept that is being studied with the aim of restoring the immune response in the tumor microenvironment. In this review, we summarize the metabolic reprogramming of various cell types present in the tumor microenvironment, with a focus on the interaction between the metabolic pathways of these cells and antitumor immunosuppression. We also discuss the main metabolic checkpoints that could provide new means of enhancing antitumor immunotherapy. [ABSTRACT FROM AUTHOR]

Squamous cell carcinoma (SCC) is an aggressive malignancy that can originate from various organs. TP63 is a master regulator that plays an essential role in epidermal differentiation. It is also a lineage-dependent oncogene in SCC. ΔNp63α is the prominent isoform of TP63 expressed in epidermal cells and SCC, and overexpression promotes SCC development through a variety of mechanisms. Recently, ΔNp63α was highlighted to act as an epidermal-specific pioneer factor that binds closed chromatin and enhances chromatin accessibility at epidermal enhancers. ΔNp63α coordinates chromatin-remodeling enzymes to orchestrate the tissue-specific enhancer landscape and three-dimensional high-order architecture of chromatin. Moreover, ΔNp63α establishes squamous-like enhancer landscapes to drive oncogenic target expression during SCC development. Importantly, ΔNp63α acts as an upstream regulator of super enhancers to activate a number of oncogenic transcripts linked to poor prognosis in SCC. Mechanistically, ΔNp63α activates genes transcription through physically interacting with a number of epigenetic modulators to establish enhancers and enhance chromatin accessibility. In contrast, ΔNp63α also represses gene transcription via interacting with repressive epigenetic regulators. ΔNp63α expression is regulated at multiple levels, including transcriptional, post-transcriptional, and post-translational levels. In this review, we summarize recent advances of p63 in epigenomic and transcriptional control, as well as the mechanistic regulation of p63. [ABSTRACT FROM AUTHOR]

During embryonic development, one of the two X chromosomes of a mammalian female cell is randomly inactivated by the X chromosome inactivation mechanism, which is mainly dependent on the regulation of the non-coding RNA X-inactive specific transcript at the X chromosome inactivation center. There are three proteins that are essential for X-inactive specific transcript to function properly: scaffold attachment factor-A, lamin B receptor, and SMRT- and HDAC-associated repressor protein. In addition, the absence of X-inactive specific transcript expression promotes tumor development. During the process of chromosome inactivation, some tumor suppressor genes escape inactivation of the X chromosome and thereby continue to play a role in tumor suppression. A well-functioning tumor suppressor gene on the idle X chromosome in women is one of the reasons they have a lower propensity to develop cancer than men, women thereby benefit from this enhanced tumor suppression. This review will explore the mechanism of X chromosome inactivation, discuss the relationship between X chromosome inactivation and tumorigenesis, and consider the consequent sex differences in cancer. [ABSTRACT FROM AUTHOR]

Numerous studies have shown that non-coding RNAs play crucial roles in the development and progression of various tumor cells. Plasmacytoma variant translocation 1 (PVT1) mainly encodes a long non-coding RNA (lncRNA) and is located on chromosome 8q24.21, which constitutes a fragile site for genetic aberrations. PVT1 is well-known for its interaction with its neighbor MYC, which is a qualified oncogene that plays a vital role in tumorigenesis. In the past several decades, increasing attention has been paid to the interaction mechanism between PVT1 and MYC, which will benefit the clinical treatment and prognosis of patients. In this review, we summarize the coamplification of PVT1 and MYC in cancer, the positive feedback mechanism, and the latest promoter competition mechanism of PVT1 and MYC, as well as how PVT1 participates in the downstream signaling pathway of c-Myc by regulating key molecules. We also briefly describe the treatment prospects and research directions of PVT1 and MYC. [ABSTRACT FROM AUTHOR]

Drought is regarded as an environmental disaster that has significantly impacted on economic and social development in recent decades, particularly in Southwest China (SWC). Here, we presented an analysis of spatiotemporal variations of meteorological drought in SWC. We computed the standardized precipitation evapotranspiration index using the Penman-Monteith equation (SPEI_pm) and explored spatiotemporal variational evolution of drought in SWC during 1962-2012 utilizing the Mann-Kendall test, continuous wavelet transform (CWT), and rotated empirical orthogonal function (REOF). We also analyzed the relationship between the rotated principal component time series (RPCs) and the 74 circulation indices. The results showed that (1) SWC displayed a dry trend at annual and seasonal scale with a 2-4-year significant period. The SWC can be divided into six sub-climate regions with different aridity and wetness features. (2) Among the six regions, the Eastern Yunnan Plateau showed an obvious dry trend while Hanzhong Basin and the Eastern Mountain Areas showed a wet trend that was not significant. There were 2-8-year periods of oscillation in general within the variation of the six regions. (3) The indices of the strength of the polar vortex in Asia (APVA) may affect the drought evolution of the whole study area. The change of drought in Eastern Yunnan Plateau and Sichuan Basin may be associated with Tibetan Plateau High. [ABSTRACT FROM AUTHOR]

Background: Bactericidal/Permeability-increasing-fold-containing family B member 1 (BPIFB1, previously termed LPLUNC1) is highly expressed in the nasopharynx, significantly downregulated in nasopharyngeal carcinoma (NPC), and associated with prognosis in NPC patients. Because metastasis represents the primary cause of NPC-related death, we explored the role of BPIFB1 in NPC migration and invasion.Methods: The role of BPIFB1 in NPC metastasis was investigated in vitro and in vivo. A co-immunoprecipitation assay coupled with mass spectrometry was used to identify BPIFB1-binding proteins. Additionally, western blotting, immunofluorescence, and immunohistochemistry allowed assessment of the molecular mechanisms associated with BPIFB1-specific metastatic inhibition via vitronectin (VTN) and vimentin (VIM) interactions.Results: Our results showed that BPIFB1 expression markedly inhibited NPC cell migration, invasion, and lung-metastatic abilities. Additionally, identification of two BPIFB1-interacting proteins, VTN and VIM, showed that BPIFB1 reduced VTN expression and the formation of a VTN-integrin αV complex in NPC cells, leading to inhibition of the FAK/Src/ERK signalling pathway. Moreover, BPIFB1 attenuated NPC cell migration and invasion by inhibiting VTN- or VIM-induced epithelial-mesenchymal transition.Conclusions: This study represents the first demonstration of BPIFB1 function in NPC migration, invasion, and lung metastasis. Our findings indicate that re-expression of BPIFB1 might represent a useful strategy for preventing and treating NPC. [ABSTRACT FROM AUTHOR]

The updated affiliations is follow: SP 1 sp NHC Key Laboratory of Carcinogenesis, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410,013, Hunan, China SP 2 sp Department of Dermatology, Xiangya Hospital, Central South University, Changsha 410,008, Hunan, China SP 3 sp Hunan Key Laboratory of Nonresolving Infammation and Cancer, The Third Xiangya Hospital, Central South University, Changsha 410,013, Hunan, China SP 4 sp The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha 410,078, Hunan, China Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Correction to: Cellular and Molecular Life Sciences (2020) 77:4325-4346 https://doi.org/10.10... The authors of the article would like to update the affiliation of the prof. [Extracted from the article]