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"Liu, Hong"
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The transcription factor FcWRKY40 of Fortunella crassifolia functions positively in salt tolerance through modulation of ion homeostasis and proline biosynthesis by directly regulating SOS2 and P5CS1 homologs
Although some WRKYs have been characterized, regulatory roles of most WRKYs remain poorly understood.
Herein, we elucidated function of FcWRKY40 from Fortunella crassifolia in salt tolerance via overexpression and virus-induced gene silencing (VIGS) and unraveled its target genes.
Overexpression of FcWRKY40 enhanced salt tolerance in transgenic tobacco and lemon, while silencing of FcWRKY40 increased salt susceptibility. Homolog genes of Salt Overly Sensitive 2 (SOS2) and Δ-1-pyrroline-5-carboxylate synthetase 1 (P5CS1) were dramatically up-regulated in transgenic lemon but down-regulated in VIGS line. Consistently, transgenic lemon displayed lower Na+ and higher proline concentrations, whereas the silenced line accumulated more Na+ but less proline. Treatment of transgenic lemon with 24-epi-brassinolide compromised salt tolerance, while supply of exogenous proline partially restored salt tolerance of the VIGS line. FcWRKY40 specifically binds to and activates promoters of FcSOS2 and FcP5CS1. FcWRKY40 was up-regulated by ABA and salt, and confirmed as a target of ABA-responsive element binding factor 2 (FcABF2). Moreover, salt treatment up-regulated FcABF2 and FcP5CS1, and elevated proline concentrations.
Taken together, our findings demonstrate that FcWRKY40 participates in the ABA signaling pathway and as a positive regulator functions in salt tolerance by regulating genes involved in ion homeostasis and proline biosynthesis.
Journal Article
Dear China : emigrant letters and remittances, 1820-1980
\"Qiaopi is one of several names given to the 'silver letters' Chinese emigrants sent home in the nineteenth and twentieth centuries. These letters-cum-remittances document the changing history of the diaspora in different parts of the world and different periods, and its ties to China. The qiaopi trade played a big part in making China transnational. This book, the first in English on qiaopi and on the origins, structure, and operations of the qiaopi trade, makes an important contribution to our understanding of modern Chinese history and to the comparative study of global migration\"--Provided by publisher.
Book
MKRN1 promotes colorectal cancer metastasis by activating the TGF-β signalling pathway through SNIP1 protein degradation
Background
The Makorin ring finger protein 1 (
MKRN1
) gene, also called RNF61, is located on the long arm of chromosome 7 and is a member of the RING finger protein family. The E3 ubiquitin ligase MKRN1 is closely linked to tumour development, but the exact mechanism needs to be elucidated. In this study, we aimed to investigate the specific mechanism and role of
MKRN1
in colorectal cancer (CRC) development.
Methods
MKRN1
expression in CRC was analysed using the Cancer Cell Line Encyclopaedia and the Cancer Genome Atlas (TCGA) databases. Rectal tumour tissues were frozen to explore the MKRN1 expression in CRC and its clinical significance. The impact of
MKRN1
on CRC cell proliferation and migration was observed using CCK8, colony formation, wound healing, and transwell assays. A combination of MKRN1 quantitative proteomics, ubiquitination modification omics analysis, and a string of in vitro and in vivo experiments revealed the potential mechanisms by which
MKRN1
regulates CRC metastasis.
Results
MKRN1
expression was significantly elevated in CRC tissues compared to paracancerous tissues and was positively linked with prognosis (
P
< 0.01).
MKRN1
downregulation inhibits CRC cell proliferation, migration, and invasion. Conversely,
MKRN1
overexpression promotes the proliferation, migration, and invasion of CRC cells. Mechanistically,
MKRN1
induces epithelial-mesenchymal transition (EMT) in CRC cells via ubiquitination and degradation of Smad nuclear-interacting protein 1 (SNIP1). Furthermore, SNIP1 inhibits transforming growth factor-β (TGF-β) signalling, and
MKRN1
promotes TGF-β signalling by degrading SNIP1 to induce EMT in CRC cells. Finally, using conditional knockout mice, intestinal lesions and metastatic liver microlesions were greatly reduced in the intestinal knockout
MKRN1
group compared to that in the control group.
Conclusions
High
MKRN1
levels promote TGF-β signalling through ubiquitination and degradation of SNIP1, thereby facilitating CRC metastasis, and supporting
MKRN1
as a CRC pro-cancer factor. The MKRN1/SNIP1/TGF-β axis may be a potential therapeutic target in CRC.
Journal Article
The National Games and National Identity in China : A History
\"The history of China's National Games reflects both the transformation of elite sport in China and wider Chinese society. This is the first book to describe the origins and development of the National Games through their dynamic relationship with Chinese politics, nationalism and identity in the modern era. Looking specifically at the role of the National Games in China's changing social, political and economic circumstances from 1910 to 2009, this book uncovers how the National Games reflected the shifts in state-led nationalist ideologies within three historical eras: the late Qing Dynasty and Republican China (1910-1948), the early People's Republic of China (1959-1979) and the People's Republic of China in the post-1980s (1983-2009). It also examines how the National Games were reformed to serve China's Olympic Strategy in the context of globalization and commercialization from the 1980s onwards. Full of original insights into archive material, each chapter sheds new light on the social, cultural and political significance of this sporting mega-event in the shaping of modern China. This is fascinating reading for anybody with an interest in the politics, history and culture of China\" -- Provided by publisher.
Book
The JA-responsive MYC2-BADH-like transcriptional regulatory module in Poncirus trifoliata contributes to cold tolerance by modulation of glycine betaine biosynthesis
• Glycine betaine (GB) is known to accumulate in plants exposed to cold, but the underlying molecular mechanisms and associated regulatory network remain unclear.
• Here, we demonstrated that PtrMYC2 of Poncirus trifoliata integrates the jasmonic acid (JA) signal to modulate cold-induced GB accumulation by directly regulating PtrBADH-l, a betaine aldehyde dehydrogenase (BADH)-like gene.
• PtrBADH-l was identified based on transcriptome and expression analysis in P. trifoliata. Overexpression and VIGS (virus-induced gene silencing)-mediated knockdown showed that PtrBADH-l plays a positive role in cold tolerance and GB synthesis. Yeast one-hybrid library screening using PtrBADH-l promoter as baits unraveled PtrMYC2 as an interacting candidate. PtrMYC2 was confirmed to directly bind to two G-box cis-acting elements within PtrBADH-l promoter and acts as a transcriptional activator. In addition, PtrMYC2 functions positively in cold tolerance through modulation of GB synthesis by regulating PtrBADH-l expression. Interestingly, we found that GB accumulation under cold stress was JA-dependent and that PtrMYC2 orchestrates JA-mediated PtrBADH-l upregulation and GB accumulation.
• This study sheds new light on the roles of MYC2 homolog in modulating GB synthesis. In particular, we propose a transcriptional regulatory module PtrMYC2-PtrBADH-l to advance the understanding of molecular mechanisms underlying the GB accumulation under cold stress.
Journal Article
Integrin signaling in cancer: bidirectional mechanisms and therapeutic opportunities
Integrins are transmembrane receptors that possess distinct ligand-binding specificities in the extracellular domain and signaling properties in the cytoplasmic domain. While most integrins have a short cytoplasmic tail, integrin β4 has a long cytoplasmic tail that can indirectly interact with the actin cytoskeleton. Additionally, 'inside-out' signals can induce integrins to adopt a high-affinity extended conformation for their appropriate ligands. These properties enable integrins to transmit bidirectional cellular signals, making it a critical regulator of various biological processes.
Integrin expression and function are tightly linked to various aspects of tumor progression, including initiation, angiogenesis, cell motility, invasion, and metastasis. Certain integrins have been shown to drive tumorigenesis or amplify oncogenic signals by interacting with corresponding receptors, while others have marginal or even suppressive effects. Additionally, different α/β subtypes of integrins can exhibit opposite effects. Integrin-mediated signaling pathways including Ras- and Rho-GTPase, TGFβ, Hippo, Wnt, Notch, and sonic hedgehog (Shh) are involved in various stages of tumorigenesis. Therefore, understanding the complex regulatory mechanisms and molecular specificities of integrins are crucial to delaying cancer progression and suppressing tumorigenesis. Furthermore, the development of integrin-based therapeutics for cancer are of great importance.
This review provides an overview of integrin-dependent bidirectional signaling mechanisms in cancer that can either support or oppose tumorigenesis by interacting with various signaling pathways. Finally, we focus on the future opportunities for emergent therapeutics based on integrin agonists.
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Journal Article
The double-edged roles of ROS in cancer prevention and therapy
Reactive oxygen species (ROS) serve as cell signaling molecules generated in oxidative metabolism and are associated with a number of human diseases. The reprogramming of redox metabolism induces abnormal accumulation of ROS in cancer cells. It has been widely accepted that ROS play opposite roles in tumor growth, metastasis and apoptosis according to their different distributions, concentrations and durations in specific subcellular structures. These double-edged roles in cancer progression include the ROS-dependent malignant transformation and the oxidative stress-induced cell death. In this review, we summarize the notable literatures on ROS generation and scavenging, and discuss the related signal transduction networks and corresponding anticancer therapies. There is no doubt that an improved understanding of the sophisticated mechanism of redox biology is imperative to conquer cancer.
Journal Article